Cardio Phys Flashcards
1
Q
systole
A
heart contraction (atrial and ventricular)
2
Q
diastole
A
heart relaxation
3
Q
cardiac muscle tissue
- cell shape
- appearance
A
- branching chains of cells
- uninucleate, striations
- intercalated discs
4
Q
microanatomy of cardiac muscle
A
- sarcolemma: plasma membrane
- sarcoplasm: cytoplasm
- sarcoplasmic reticulum: ER
- t tubules: unique to cardiac muscle
- myofibrils
- myofiliaments
5
Q
What are the 2 myofilaments
A
- myosin
- actin
6
Q
What is the thick filament?
A
-myosin
7
Q
myosin characteristics
A
- A band
- made up of a globular head and tail
- has ATPase binding site
- has actin binding site
8
Q
what is the thin filament?
A
-actin
9
Q
actin characteristics
A
-globular actin (G): individual subunits of protein that forms fibrous actin (F)
10
Q
tropomyosin
A
double stranded filament that winds around actin
11
Q
troponin
-what does it bind
A
- TnI: binds actin
- TnT: bind tropomyosin
- TnC: binds Ca++
12
Q
Cardiomyocyte contractile cycle:
step 1
A
- Ca++ binds TnC
- conformational change
- tropomyosin displaced from actin binding sites
13
Q
Cardiomyocyte contractile cycle:
step 2
A
-crossbridge formation occurs through hydrolyzation of ATP
14
Q
Cardiomyocyte contractile cycle:
step 3
A
- power stroke moves actin filament toward center of sarcomere
- ADP released from myosin heads
15
Q
Cardiomyocyte contractile cycle:
step 4
A
- actin release w/ ATP binding myosin
- myosin heads cocked back
16
Q
Cardiomyocyte contractile cycle:
step 5
A
- cycle continues until cellular Ca++ levels decrease b/c Ca dissociates from troponin
- tropomyosin returns to original conformation that blocks actin binding site
17
Q
summary of cardiac muscle contraction
A
- sarcomeres shorten
- myosin crossbridges bind actin
- draws actin to center of sarcomere
- requires Ca++
18
Q
What is the condition of the sarcomere during the relaxed state?
A
- low ICF Ca++
- tropomyosin blocks actin/myosin from binding
19
Q
depolarization wave in contraction (function of Ca++)
A
- Ca++ released to ICF
- Ca++ binds troponin (TnC)
- conformational change removes tropomyosin from actin to reveal myosin binding site
- myosin crossbridge binds actin
20
Q
How do the filaments slide during cardiac muscle contraction?
A
- ATPase activity of myosin head hydrolyzes ATP to release energy to pivot head
- slides filaments together
- multiple attach and release phases shorten sarcomere
21
Q
When does filament sliding end?
A
when the stimulation ends
22
Q
What 2 main things are needed to have sliding filaments/contraction?
A
- Ca++
- ATP
23
Q
properties of a cardiac myocyte
A
- striations
- actin and myosin
- involuntary control
- autonomic
- hormonal control through epi
24
Q
What are the two different heart cell types?
A
- contractile myocytes
- nodal cells
25
contractile myoctes
- bulk of the heart
| - act as a syncytium d/y attachment and intercellular communication
26
nodal cells
- modified myocytes
- non-contractile
- initiate and conduct electrical impulse from atria to ventricles to stimulate myocardial contraction
27
2 pathways involved with the SA node
- Intra-atrial pathways
| - internodal pathways (SA to AV)
28
intra-atrial pathways (2)
1. Bachmann bundle
| 2. atrial myocytes
29
internodal pathways (3)
1. anterior tract
2. Wenckebach tract
3. Thorel tract
30
bundle of His
- pathway through the septum
- branches into LBB and RBB
- LBB: anterior & posterior fascicle
- RBB
31
Purkinje fibers
retrograde system that travel back up the heart walls
32
What is unique to the action potential in ventricular cardiac myocytes?
- depolarization is prolonged
| - not just a spike like normal action potentials
33
What is the point of the prolongation/plateau in the cardiac myocyte action potential? And what causes it?
- to sustain the contraction of the ventricles
| - Ca++ channels open and some K channels close to allow the prolongation
34
What characteristic is unique to the SA and AV nodes?
-prepotential aka pacemaker potential
35
What causes repolarization?
-influx of K+
36
SA node
- location
- rate
- RA at junction w/ SVC
| - 60-100 BPM
37
AV node
- location
- rate
- RA at posterioinferior area of interatrial septum
| - 40-60 BPM
38
Purkinje fibers and ventricular myocytes
- location
- rate
- throughout the ventricles
| - 20-40 BPM
39
What part of the nervous system controls the heart?
ANS
40
PSNS vs SNS outflow originations
- PSNS: craniosacral
| - SNS: thoracolumbar
41
PSNS neurotransmitter
ACh
42
Ach acts on what types of receptors?
-cholinergic
43
What are the 2 types of cholinergic receptors?
- muscarinic
| - nicotinic
44
SNS neurotransmitter
- from the preganglionic
- from the postganglionic
- preganglionic: Ach
| - postganglionic: norepinephrine
45
norepinephrine activates what receptors?
adrenergic
46
Adrenergic receptor types
- alpha 1
- alpha 2
- beta 1
- beta 2
47
What receptor is found on cardiac muscle?
-beta 1
48
SA node is under PSNS control through what?
Vagus N.
49
AV node is under PSNS control through what?
Vagus N.
50
What is vagal stimulation
- Ach to (M2) muscarinic receptors
- Decreases Ca++ channels prevents depolarization
- Increase K+ channels to hyperpolarize mb
- firing rate decreases
51
Which has a greater effect on the heart, PSNS or SNS?
-SNS
52
SNS control of the heart
- fibers innervate nodes
- release norepinephrine to beta-1 receptors
- increases L channel opening and Ca++ influx
- increases rapidity of depolarization
- SNS drives heart rate
53
In the spread of cardiac excitation, what happens when the SA node depolarizes?
- spreads radially through atria
- converges on AV node
- takes about .1 seconds
54
What is the nodal delay at the AV node?
0.1 seconds
55
what is the cardiac cycle
- all of the events associated w/ blood flow through the heart during 1 complete heart beat
- divided into systole and diastole
56
blood flows through the heart based on __________?
pressure changes
57
AV valves
- tricuspid
| - mitral
58
AP valves
- aortic
| - pulmonic
59
During late diastole:
- valves
- pressure
- blood filling
- % of filling
- AV valves open
- AP valves closed
- pressure is low
- blood fills chambers
- 70% of ventricular filling
60
During atrial systole
- valves
- atria
- pressure
- AV valves open
- AP valves closed
- atria contract (p wave), atrial pressure rises propelling blood to ventricles
- aortic pressure is around 80mm Hg = diastolic pressure
61
During ventricluar systole:
- valves
- path
- phases
- AV valves open
- AP valves closed
- begins at QRS
- as atria relax, vent. systole begins
- biphasic
- isovolumetric ventricular contraction phase
62
during isovolumetric ventricular contraction phase, what shuts the AV valves?
-ventricular pressure rises
63
S1 "LUB" is created by what?
-AV valves shutting (AP valves still shut)
64
pressure during isovolumetric ventricular contraction
- blood is contained in ventricles
- remains until the pressure exceeds that of aorta and pulmonary artery
- aortic pressure is around 90mm Hg
65
Ventricular systole:
- valves
- phase
- AV valves closed
- AP valves closed
- ventricular ejection phase
66
ventricular ejection phase
- ventricular pressure exceeds great arteries
- AV leaflets are pressed up, increasing arterial pressure
- AP valves open, ventricular blood is ejected
- aortic pressure is at peak - 120mm Hg
- i.e peak systolic pressure
67
two parts of early diastole
- protodiastole
| - isovolumetric diastole
68
protodiastole
- ventricular pressures fall
| - AP valves flap closed
69
what creates the S2 ("DUB") sound?
AP valves flap closed
70
isovolumetric diastole
- ventricular pressures continue to fall
- ends when arterial pressure exceeds ventricular pressure
- AV valves sucked open
- enter ventricular filling phase
71
Length cardiac cycle
-cardiac cycle: .8 sec
72
length of atrial and ventricular systole
- atrial systole: .1 sec
| - ventricular systole: .3 sec
73
length of diastole
-diastole: .4 sec
74
end-diastolic ventricular volume (EDV)
- at the end of relaxation, AV valves open, ventricles have filled
- EDV is this volume
75
end-systolic volume (ESV)
volume after contraction
76
stroke volume (SV)
how much was moved during the contracted stroke
77
SV equation
SV = EDV - ESV
78
ejection fraction
- %EDV ejected per stroke
| - good indicator of ventricular function
79
ejection fraction equation
EF = SV/EDV
i.e: EF = EDV - ESV/EDV x 100%
80
ejection fraction equation in word form
amount of blood pumped out of the ventricle divided by the total amount of blood in the ventricle
81
ejection fraction values:
- normal
- below normal
- low
- normal: 50-65%
- below normal: 36-49%
- low: 35%
82
if EF is normal:
the heart is pumping normally and can deliver an adequate supply of blood to the body and brain
83
if EF is below normal:
could indicate that the heart is not pumping well enough to meet the body's needs
84
if EF is low:
- indicates a weakened heart muscle and poorly pumping heart
- low EF number increases the risk of sudden cardiac arrest
85
cardiac cycle
she gave various charts to review the overall cycle. slides 36-38
86
arterial pulse is felt during what part of the cardiac cycle?
-ventricular systole: it creates the highest systolic pressure which travels along the arteries
87
nl arterial pulse
60-100 bpm
88
nl newborn (0-3 mo.) pulse
100-150
89
nl infant pulses
- 3-6 mo: 90-120
| - 6-12 mo: 80-120
90
nl children (1-10yrs) pulse
70-130
91
Dicrotic notch
- vibrations caused as aortic valve snaps shut
- at end of ventricular systole (DUB)
- secondary upstroke in descending part of pulse
- measurable but not palpable
92
jugular venous pressure (JVP)
- indirectly visualized by observing jugular pulse
- atrial pressure increases during atrial systole and through isovolumetric phase of V systole
- falls when AV valves open
- atrial pressure changes are transmitted to great viens (jugular)
93
what can be a cause of JVD
heart failure
94
S1 LUB sound
- AV valve closure
- onset of V systole
- louder, longer, more resonant
- .15 sec
- 25-45 mHz
95
S2 DUB sounds
- semilunar valve closure
- beginning of V diastole
- shorter and sharper sound
- .12 sec
- 50 mHz
96
S3 heart sound
- 1/3 of the way through diastole
- "kentucky"
- nl in young d/t rush of vent. filling
- abnl in mitral regurg or heart failure
97
S4 heart sound
- immediately before S1
- abnl
- high atrial pressure or ventricular stiffness
98
mitral valve closes slightly before what?
tricuspid
99
aortic valve closes just before what?
pulmonary
100
what is the physiological split of S2?
-you hear A before P during deep inspiration
101
bruit
-abnl sounds auscultated over a blood vessel
102
carotid bruit
- might be innocent
- lumen is reduced d/t atherosclerosis
- can cast emboli and result in cerebral ischemia
- carotid endarterectomy if >50%
103
CO =
amount of blood in L pumped out by each ventricle in 1 min.
CO = HR x SV
104
stroke volume =
vol. of blood ejected by V per contraction
105
what is the approximate blood vol in the cardiovascular system?
5 L
106
cardiac reserve
-ability of heart to push its CO above nl to meet needs
107
what is nl cardiac reserve?
4 X CO
(20L)
-athletes can be 35L
108
changes in CO are accomplished by what?
-regulation of HR and or SV
109
SV equation
SV = EDV - ESV
110
EDV
- length of ventricular diastole
| - venous pressure
111
ESV
- arterial blood pressure
| - force of vent. contraction
112
Frank-Starling Law
- energy of contraction is proportional to the initial length of the cardiac muscle fiber
- layman terms: the more you can stretch, the more you can contract
113
in Frank Starling law, the length of the muscle fiber is proportional to what?
EDV
114
the most important factor in stretch is what?
- venous return increasing EDV
| - AKA preload*
115
anything increasing EDV also increases what?
- SV
| - CO
116
frank starling curve
-shows relationship b/w ventricular SV and EDV
117
increasing CO in frank starling curve
- slow HR
| - exercise
118
decreasing CO in frank starling curve
- high HR
- blood loss
- heart dz
119
____ is the single most important factor affecting SV, and therefore CO.
EDV
120
factors that can affect EDV
- healthy pericardium
- atrial systole
- vent. compliance
- blood vol.
- venous constriction
- systolic dysfunction
- diastolic dysfunction
121
afterload
- pressure on the wall of the left vent. during ejection
| - end load or pressure against which the heart contracts to eject blood (resistance)
122
what increases afterload?
-HTN
-aortic stenosis
(b/c vent. has to work harder)
123
contractility
- ability of the heart muscle to contract
- the effect of sympathetic stimulation on heart
- usually increases Ca++ availability to myocardium, promoting crossbridge activity and therefore stroke
- increases conduction as well
124
what is the most important extrinsic factor affecting SV?
contractility
125
contractility is what effect?
- ionotropic
| - think change in ions
126
positive ionotropic effects
- increase contractility
- SNS via catecholamines (E, NE, dopamine)
- caffeine
- theophylline
- digitalis
- insulin
127
negative ionotropic effects
- decrease contractility
- vagal stimulation
- hypercapnia
- hypoxia
- acidosis
- agents used to decrease cardiac workload
- beta blockers
- Ca++ channel blockers
- quinidine
- procainamide
128
factors affecting HR
- autonomic innervation
- hormones
- fitness level
- age
129
factors affecting SV
- heart size
- fitness level
- gender
- contractility
- duration of contraction
- preload (EDV)
- afterload (resistance)
130
chronotropy
HR
131
dromotropy
conduction
132
ionotropy
- contractility (beta 1)
| - pre and after load (beta 2)
133
lusitropy
diastolic relaxation
134
myocardial oxygen consumption correlation with what?
ventricular work
135
myocardial O2 is based on what?
- SV
| - mean arterial pressure
136
what causes greater O2 consumption, pressure work or volume work?
pressure work
137
what causes greater O2 consumption, afterload or preload?
afterload
