Cardiac Impulse Flashcards
1
Q
where in the body are the electrical signal which control the heart stimulated
A
within the heart
2
Q
is the heart capable of beating in the absence of external stimuli
A
yes
3
Q
what is autorhythmicity
A
heart’s ability to beat in the absence of external stimuli
4
Q
where does excitation of the cells normally originate
A
pacemaker cells in the sino-atrial node
5
Q
what does the cluster of specialised cells in the SA node initiate
A
heart beat
6
Q
where is SA node located
A
upper right atrium, close to where the superior vena cava enters the right atrium
7
Q
does the SA node normally drive the pace for the ENTIRE heart
A
yes
8
Q
what is sinus-rhythm
A
when a heart is controlled by the sino-atrial node
9
Q
describe the stability of the cells in the SA not
A
not stable as do not have a resting membrane potential- slowly drift towards depolarisation
10
Q
what potential do cells in the SA node exhibit
A
spontaneous pacemaker potential
11
Q
does the spontaneous pacemaker potential create action potential? explain answer
A
yes- spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential
12
Q
in pacemaker cells in the permeability to K+ always constant
A
no- changes between action potentials
13
Q
define pacemaker potential
A
the slow depolarisation of membrane potential to a threshold
14
Q
what physiological factors contribute to pacemaker potential
A
decreased K+ efflux (slowing of accumulation of pos ions leads to depolarisation), Na+ and K+ influx, transient Ca++ influx
15
Q
what is the funny channel
A
Na+ and K+ influx
16
Q
via which type of channels does Ca++ influx
A
T-type Ca++ channels
17
Q
what does potassium efflux at normal rate trigger
A
hyper polarisation
18
Q
what happens when a pacemaker cells reaches its threshold
A
cell enters rising phase of action potential
19
Q
what is the threshold for a pacemaker cell
A
-40mV
20
Q
what is the rising phase of the action potential
A
depolarisation caused by activation of long lasting- influx of Ca++ via L-type Ca++ channels
21
Q
what follows the rising action potential
A
falling phase of action potential
22
Q
what is the falling phase of action potential
A
re-polarisation caused by inactivation of L-type Ca++ channels and activation of K+ channels (decreased Ca++ influx, increased K+ efflux)
23
Q
does action potential have to spread to all cardiac muscle
A
yes
24
Q
how does action potential travel from the sino-atrial node to the atrioventricular node
A
cell to cell conduction
25
describe the anatomy of the atrioventricular node
starts as bundle of specialised cardiac cells (bundle of his), then separates into left and right branches, then further into purkinje fibres
26
how does the current flow from cell to cell
via gap junctions- desmosome
27
where does cell-to-cell spread of excitation carry action potential across whole heart
from SA to AV, from SA through both atria, within ventricles
28
why can action potential travel through a gap junction
as it has lower resistance
29
what is the AV node
small bundle of specialised cardiac cells
30
where is the AV node located
at the base of the right atrium, just above the junction of atria and ventricles
31
how does the AV node connect the artia and ventricles
ONLY point of contact between atria and ventricles- action potential can only go through AV node and not fibrous ring separating chambers
32
describe the the specialised AV node cells
small in diameter- slow conduction velocity
33
what other types of pathways all conduction from SA node to the AV node
internodal pathways
34
why is conduction delayed in the AV node
allows atrial systole (contraction) to precede ventricular systole
35
what allows rapid spread of action potential to the ventricles
bundle of his, its branches and the network of Purkinje fibres
36
how does action potential spread within the ventricular muscle
cell-to-cell conduction
37
is the action potential in contractile cardiac muscles cells the same as pacemaker cells
no v different
38
describe the resting membrane potential of atrial and ventricular myocytes
remains at -90mV until the cell in excited
39
what happens to the action potential of a cardiac myocyte when it is excited
enters rising phase of action potential- depolarisation caused by fast Na+ influx
40
what effect does the rising phase of a mycotyes action potential have on membrane potential
rapidly reverses it to +20mV
41
what is the rising phase of action potential in contractile cardiac muscles cells known as
phase 0
42
phases of ventricular muscle action potential; summarise phase 0
fast Na+ influx
43
phases of ventricular muscle action potential; summarise phase 1
closure of Na+ channels and transient K+ efflux
44
phases of ventricular muscle action potential; summarise phase 2
mainly Ca++ influx
45
phases of ventricular muscle action potential; summarise phase 3
closure of Ca++ channels and K+ efflux
46
phases of ventricular muscle action potential; summarise phase 4
resting membrane potential
47
what phase of ventricular muscle action potential is the plateau phase
phase 2
48
describe the plateau phase of ventricular muscle action potential
when membrane potential is maintained near the peak of action potential for a few hundred milliseconds
49
what is the plateau phase mainly due to
influx of Ca++ through L-type Ca++ channels
50
what happens after the plateau phase
the falling phase of action potential- re-polarisation
51
what causes the falling phase of ventricular muscle action potential
(re-polarisation) caused by inactivation of Ca++ channels and activation of K+ channels
52
what does the falling phase of ventricular muscle action potential result in
k+ efflux
53
what part of the nervous system influences heart rate
autonomic nervous system
54
how does sympathetic stimulation affect heart rate
sympathetic stimulation increases heart heart
55
how does parasympathetic stimulation affect heart rate
decreases heart rate
56
what is the parasympathetic supply to the heart
vagus nerve
57
what is the vagal tone
vagus nerve exerts continuous influence on the SA node under resting conditions
58
what is the dominate influence on the SA under normal resting conditions
vagal tone
59
what does the vagal tone do to the heart rate
slows it from the intrinsic heart rate (approx 100bpm) to a normal heart rate (approx 70bpm)
60
what can intrinsic heart rate also be known as
tachycardia
61
what is a normal resting heart rate
between 60 and 100 BPM
62
What is bradycardia
a heart rate less than 60 BPM
63
what is tachycardia
heart rate more than 100 BPM
64
Does the vagus nerve supply both nodes
yes
65
what does vagal stimulation do to heart rate
slows it
66
what does vagal stimulation do to AV nodal delay
increases it
67
what is the neurotransmitter of the vagus nerve and what does it act through
acetyle choline, muscarinic M2 receptors
68
what is atropine
competitive inhibitor of acetylcholine
69
when is atropine used
in extreme bradycardia to speed up the heart
70
what is the effect of vagal stimulation on pacemaker potentials
cell hyperpolarises- longer to reach threshold= slope of pacemake potential decreases + frequency of AP decreases= negative chronotropic effect
71
what is a negative chronotropic effect
anything that slows HR- e.g. parasympathetic stimulation
72
what do the cardiac sympathetic nerves supply
SA node, AV node, myocardium
73
what effect does sympathetic stimulation have on HR
increases HR
74
what effect does sympathetic stimulation have on AV nodal delay
decreases it
75
what else does sympathetic stimulation affect in the heart
force of contraction- increases it
76
what is the neurotransmitter of the sympathetic nervous system and what does it act through
noradrenaline, acting through Beta1 adrenoceptors
77
what effect does noradrenaline have on the potential of pacemaker cells
slope of pacemaker potential increases, reaches threshold quicker, frequency of action potentials increases= positive chronotropic effect
78
what effect does noradrenaline have on pacemaker cell K+ influx
decreases
79
what effect does acetyl-choline have on pacemaker cell K+ influx
increases it
80
what effect does acetyl-choline have on pacemaker cell Na+ and Ca++ influx
decreases it
81
what effect does noradrenaline have on pacemaker cell Na+ and Ca++ influx
increases it
82
what is an ECG
record of depolarisation and re-polarisation cycle of cardiac muscle obtain from electrical current that move across heart and can be detected on skin surface
83
where do you attach lead one in an ECG
RA (right arm) to Left arm (LA)
84
where do you attach lead two in an ECG
RA to LL (left Leg)
85
where do you attach lead three in an ECG
left arm to left leg
86
which limb is earthed
right leg
87
what does P mean in an ECG
atrial depolarisation
88
what does QRS complex mean in an ECG
ventricular depolarisation (masks atrial repolarisation)
89
what does T mean in an ECG
ventricular repolarisation
90
what does PR interval mean in an ECG
largely AV node display
91
what does ST segment mean in an ECG
ventricular systole
92
what does TP interval mean in an ECG
diastole
93
what is the area between two cardiac cells called
intercalated disc
94
describe arrangement of cardiac muscle
striated
95
what causes striation
regular arrangement of contractile proteins
96
are there neuromuscular junctions in the cardiac muscle, explain answer
no as capable of generating own action potential
97
what is the function of desmosomes within the intercalated discs
provide mechanical adhesion between adjacent cells and ensure tension developed by one cell is transmitted to the next
98
what is a myofibril
contractile units of muscle- many eithin each muscle fibre
99
describe the components of myofibrils
alternating segments of thick (myosin) and thin (actin) protein filaments
100
what causes the darker appearance of muscle
the myosin (thick filaments)
101
what are sarcomeres
functional unit of the tissue- what actin and myosin are arranged into
102
what produces muscle tension
sliding of actin filaments on myocin filaments
103
what is force generation dependant on
ATP-dependant interactionbetween thick (myosin) and thin (actin) filaments. cannot happen in absence of ATP and calcium
104
is ATP required for both contraction and relaxation
yes
105
describe the route of ATP in muscle contraction
attaches to myosin head. splits in ADP and Pi creating energised myosin head. depending on presence of Ca2+ myosin enters either resting (absent) or binding (present) state. ATP released as myosin binds and myosin slides along actin.
106
why is there no cross bride binding in a relaxed muscle fibre
as the binding site on actin is physically covered by the troponin-tropomyosin complex
107
what does the binding of actin and myosin trigger
power stroke that pulls
| thin filament inward during contraction
108
what allows crossbridges to form in an excited muscle fibre
Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross bridge binding site
109
where in the calcium release from
sarcoplasmic reticulum (SR)
110
in cardiac muscle what is the release of Ca++ from SR dependant on
presence of extra-cellular Ca++
111
where is most of the Ca++ in a resting muscle cell
most outwith cell, intracellular Ca++ stored within SR
112
what happens to the calcium concentration during the plateau phase of ventricular muscle action potential
Ca++ influx through L- type Ca++ channels into cardiac myoctyes
113
what does the calcium influx during the plateau phase also stimulate
release of more calcium from SR (CICR)
114
what does the high intracellular calcium combined activate
contractile machinery (stimulates formation of cross bridges)
115
what happened to Ca++ after action potential passes
Ca++ re-sequestered in SR by Ca++-ATPase and the heart muscle relaxes
116
what does the long refractory period in ventricular muscle action and tension prevent
tetanic contraction
117
does skeletal muscle have the same refractory period
no
118
what is a refractory period
period following an action potential in which it is not possible to produce another action potential
119
what phase helps create refractory period
plateau
120
describe the Na+ channels during the plateau phase
in depolarised closed state
121
describe the K+ channels during the descending phase of the action potential
open, cannot be depolarised
122
what is stroke volume
the volume of blood ejected by each ventricle per heart beat
123
when is stroke volume ejected
contraction of ventricular muscle
124
how is stroke volume calculated
end diastolic volume (EDV) - end systolic volume (ESV)
125
what is stroke volume regulated by
intrinsic and extrinsic mechanisms
126
where do intrinsic mechanisms originate from
within the heart muscle (organ) itself
127
where do extrinsic mechanisms originate from
nervous and hormal control
128
where does the right side of the heart eject its stroke volume into
PA
129
where does the left side of the heart eject its stroke volume into
the aorta
130
what are changes in stroke volume brought about by
diastolic length of myocardial fibres
131
what is the diastolic length of the myocardial fibres determined by
volume of blood within each ventricle- end diastolic volume
132
what determines cardiac preload
end diastolic volume
133
what determines end diastolic volume
venous return to the heart
134
what does the frank starling law describe
relationship between venous return, end diastolic volume and stroke volume
135
describe the frank starling law
the more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)
136
when is maximum force generated by a muscle
when fibres are a optimum length
137
what does the stretch of muscle fibres also increase the affinity for
Ca++
138
in skeletal muscle when are the fibres at optimum
when at rest
139
in cardiac muscle when are the fibres at optimum
achieved by stretching the muscle
140
if a venous return to right atrium increases what happens to the EDV of the right ventricle
increases (increased SV into pulmonary artery)
141
what happens to the EDV of left ventricle when venous return to left atrium from pulmonary vein increases
increases (increased SV into aorta)
142
what is afterload
the resistance into which heart is pumping
143
what happens at first if after load is increased and why
EDV increases as heart unable to eject full SV
144
what happens if increased afterload continues to exist (e.g. untreated hypertension)
eventually ventricular muscle mass increases (ventricular hypertrophy) to overcome resistance
145
what does the frank-starling mechanism do to compensate for decreased stroke volume
increased force of contraction
146
what does sympathetic stimulation do to force of contraction
increases it
147
what is a positive inotropic effect
increased force of contraction
148
does noradrenaline have a pos or neg inotropic effect
pos
149
what does noradrenaline do to left ventricular pressure
increases
150
what effect does sympathetic stimulation of ventricular contraction have on calcium
activates Ca++ channels- greater Ca++ influx
151
what mediates the effect of sympathetic stimulation on ventricular contraction
cAMP
152
what happens to the rate of left ventricular pressure change during stole when under sympathetic stimulation
increases, happens quicker, faster contraction, faster heart rate
153
what happens to rate of ventricular relaxation (and therefore duration of diastole) when under sympathetic stimulation
increases, reduced rate
154
what happens to the frank starling curve when ventricular contraction under symp stim
shifted to the right
155
what effects do positive and negative inotropic agents have on the frank staling curve
```
pos= shifts to left
neg= shifts to right
```
156
what inotropic effect will heart failure have on the frank staling curve
shift to right as smaller stroke volume
157
what effect does vagal stimulation have on ventricular contraction and why
major influence on rate, not force of contraction- as very little innervation on ventricles so has little effect on SV
158
what releases adrenaline and noradrenaline (hormones) and what effect do they have
adrenal medulla- inotropic and chronotropic effect
159
what is cardiac output
volume of blood pumped by each ventricle per minute
160
how is cardiac output calculated
SV x HR
161
what is the normal resting CO
5 litres per minute
