Cardiovascular Physiology Flashcards
1
Q
the heart
A
- size of fist
- between ribs 2-5
- 2/3 length at midline
- weighs 10 oz.
- beats 3 billion times in lifetime (80 years)
2
Q
anatomical axis of heart
A
45 degrees
3
Q
what are the four chambers of the heart?
A
- right atrium
- left atrium
- right ventricle
- left ventricle
4
Q
what are the four valves of the heart?
A
- 2 AV valves
- 2 semilunar valves
5
Q
papillary muscles
A
attach to tendinous cords
6
Q
tendinous cords
A
attack to cusps of AV valves to keep them from prolapsing into atria
- don’t pull valves open
- act only to limit movement
7
Q
cardiac muscle
A
myocardium
8
Q
what are the semilunar valves?
A
- aortic valve
- pulmonary valve
9
Q
what are the AV valves?
A
- bicuspid valve
- tricuspid valve
10
Q
semilunar valves
A
3 cusps with “pockets”
- when blood flows back, closes valve
11
Q
stenosis
A
narrowed opening due to scar tissue
- when blood is flowing through
- makes whistle sound
12
Q
stenosis causes
A
- increased BP causing increased wear / tear
- rheumatic fever = antibodies attack valves
13
Q
valvular insufficiency
A
valves don’t close properly blood leaks backward (regurgitation)
- makes a gurgling sound
14
Q
what is the mot commonly replaced valve?
A
mitral value
bicuspid valve
15
Q
pulmonary
A
- right side
- low pressure
- about 10 mm Hg
16
Q
systemic
A
- left side
- high pressure
- about 110 mm Hg
17
Q
blood flow through the heart
A
- superior and inferior vena cava
- right atrium
- tricuspid value
- right ventricle
- pulmonary valve
- pulmonary trunk
- R/L pulmonary artery
- lungs
- pulmonary veins
- left atrium
- bicuspid valve
- left ventricle
- aortic valve
- aorta
- systemic capillaries
18
Q
cardiac muscle tissue
A
- short, branched cells connected by intercalated discs
- involuntary
- aerobic respiration only
- –> lots of mitochondria (no fatigue)
19
Q
syncytium
A
intercalated discs contain gap junctions so that cells contract in unison
20
Q
all three muscle types are similar by:
A
- sliding filaments
- ATP power
- elevated Ca+2 triggers
21
Q
cardiac muscle is like skeletal by:
A
- sarcomeres
- striations
- troponin
- t-tubules
- SR Ca+2
22
Q
cardiac muscle is like smooth by:
A
- small, single nucleus
- pacemaker cells
- gap junctions (syncytium)
- autonomic/hormones modulate
- Ca+2 entry from outside
23
Q
EC coupling in cardiac muscle
A
- Ca+2 flow thru the DHPR (L-type Ca+2 channel) opens the RyR releasing Ca+2 from the SR. The Ca+2 induces additions Ryr channels to open
24
Q
CIRI
A
Ca+2 induced Ca+2 release
- positive feedback
25
autorhythmic cells (pacemaker cells)
- <1% of cells
- determine HR
- myogenic
26
myogenic
- can contract without nervous system input
- beat on its own
- ex: SA node (75 bpm) , AV node (45 bpm)
27
conducting cells
spread electrical stimulus
- ex: bundle of his (AV bundle) , bundle branches, purkinje fibers
- all of these also have pacemaker activity
28
contractile cells
- 99%
- myocardium
- all have gap junctions --> AP spreads from one cell to another
- every heart cell contracts with every beat
29
electrical conduction system
1. SA node fires
2. excitation spreads through myocardium
- atrial contraction (systole)
3. AV node fires
4. excitation spreads down AV bundle
5. purkinje fivers distribute excitation through ventricular myocardium
- ventricular contraction
- 3-5 are fast
30
electrical conduction through myocardium
1. atria contract in unison
2. delay at AV node (ventricles fill)
3. ventricles contract in unison
31
sinus rhythm
normal heartbeat triggered by the SA node
| - about 75 bpm
32
ectopic focus
any region of spontaneous firing other than SA node
33
nodal rhythm
- AV node produces this
- backup pacemaker
- about 45 bmp
34
bundle of his/bundle branches/purkinje fibers
- < 35 bpm
| - not fast enough to sustain life
35
pacemaker potentials of nodal cells
- Na+ enters = Na+ leak channels always open = no stable RMP
- Ca+2 enters (depolarization) = VG Ca+2 channels
- myogenic (beats on its own)
36
action potential in contractile cells
1. only depolarize when stimulated (no potential activity) VG Na+ channel
2. Na+2 inflow depolarizes membrane and triggers opening of more Na+ channels (positive feedback) and rapid increase in voltage change
3. Na+ channels close and voltage peaks at +30 mV
4. Ca+2 and K+ channels open and inflow of Ca+2 prolongs repolarization (K+ out)
5. Ca+2 channels close and K+ outflow returns membrane to RMP
- 99% of myocardium
37
cardiac muscle AP
- have long refractory period to prevent tetanus
| - no temporal summation
38
electrocardiogram (EKG)
- composite recording of all electrical activity in heart
- not directly APs
- used to determine heath of heart
- HR, regularity, size, position of chambers, damage
39
Einthoven's Triangle
combination of 12 leads uses a different combination of reference and recording electrodes to provide different angles for "viewing" the heart
40
standard limb leads
- lead I
- lead II
- lead III
41
augmented limb leads
- aVR
- aVL
- aVF
42
pericardial (chest) leads
use limb leads combined into a reference point at the center of the heart
- V1 - V6
43
P wave
atrial depolarization
44
PQ segment
- atrial contraction
| - delay at AV node
45
QRS complex
- ventricular depolarization
| - atrial repolarization
46
ST segment
ventricular contraction
47
T wave
ventricular repolarization
48
TP interval
diastole
49
average MEA
59˚
50
normal range MEA
-30˚ - +110˚
51
MEA
tells us the net direction depolarization is heading
52
QRS complex is highly positive
electrical axis is parallel to that lead
| - normal
53
QRS complex is highly negative
electrical axis is in opposite direction to that lead (inverted QRS)
54
QRS complex is isoelectric
perpendicular to that lead
55
left axis deviation (LAD)
MEA < -30˚
56
causes of left axis deviation
1. left ventricular hypertrophy
2. right ventricular destruction
3. altered body structure
57
left ventricular hypertrophy:
- from increased BP
| - mitral / aortic valve stenosis
58
right ventricular destruction:
from heart attack (myocardial infarction --> MI)
59
altered body structure from LAD
short, obese
60
pathologic hypertrophy
either ventricle, the axis will shift in direction of hypertrophied ventricle
61
right axis deviation (RAD)
MEA > 110˚
62
causes of right axis deviation
1. right ventricular hypertrophy
2. left ventricular destruction
3. altered body stature
63
right ventricular hypertrophy
- caused by pulmonary hypertension
| - tricuspid / pulmonary stenosis
64
left ventricular destruction
heart attack (MI)
65
altered body structure from RAD
extremely tall, thin
66
bradycardia
HR < 60 bpm
| - increased TP interval
67
tachycardia
HR > 100 bpm
| - decreased TP interval
68
artificial pacemaker
surgically implanted to provide electrical stimulus (artificial depolarization) to take over for either SA node or AV node
69
types of artificial pacemakers
1. constant pacemaker
| 2. demand pacemaker
70
constant pacemaker
constantly fire and set HR
71
demand pacemaker
fires when needed
72
when do you need a pacemaker
- possibly if SA node fails
- any exertion requiring increased HR would be difficult to sustain
- ALWAYS if AV node fails = only electrical link to ventricles
73
function of heart
to create pressure gradient
74
how does pressure flow?
high pressure to low pressure
75
pressure of atria
low
76
pressure of arteries
high
77
pressure of ventricles
varies
78
AV valves open
P atria > P ventricles
79
AV valves closed
P ventricles > P atria
80
SL valves open
P ventricles > P arteries
81
SL valves closed
P arteries > P ventricles
82
phase 1 of cardiac cycle
- TP interval
- ventricular filling --> blood flows into ventricles
- atria relaxed
- ventricles relaxed
- P wave --> PQ segment
- atria contract
- ventricles relaxed
- AV valves: open
- aortic and pulmonary valves: closed
- P atria > P ventricles
- EDV
83
End diastolic volume (EDV)
about 130 mL
84
phase 2 of cardiac cycle
- isovolumetric ventricular contraction
- QRS complex --> beginning of ST segment
- atria relaxed
- ventricles contract
- AV valves: closed
- ---> close first
- aortic and pulmonary valves: closed
- P ventricles > P atria
- P ventricles < P arteries
85
isovolumetric ventricular contraction
- same volume --> tension but no blood flow
- volume stays same because all valves closed
- as P ventricles increase, AV valves closes P ventricles > P atria
86
phase 3 of cardiac cycle
- ventricular ejection = blood flows out of ventricle
- ST segment
- atria relaxed
- ventricles contract
- AV valves: closed
- aortic and pulmonary valves: open
- P ventricles > P arteries
- stroke volume
87
stroke volume average
about 70 mL
88
phase 4 cardiac cycle
- isovolumetric ventricular relaxation
- T wave
- atria relaxed
- ventricles relaxed
- AV valves: closed
- aortic and pulmonary valves: closed
- P ventricules < P arteries
- end systolic volume
89
end systolic volume
about 60 mL
90
isovolumetric ventricular relaxation
- as P ventricle decreases, SL valves close
| - volume stays because all valves closed
91
end systolic volume
about 60 mL
92
AV valves close
"lub"
93
SL valves close
"dub"
94
pressure-volume loop: one cardiac cycle
left ventricular pressure (LVP) is plowed against left ventricular volume (LVV) at multiple time points during a complete cardiac cycle
95
ESV equation
EDV - SV = ESV
96
pulmonary edema
1. right ventricular output exceeds left ventricular
2. pressure backs up
3. fluid accumulates in pulmonary tissue
- left ventricular failure
97
systemic edema
1. left ventricular output exceeds right ventricular output
2. pressure backs up
3. fluid accumulates in systemic tissue
- right ventricular failure
- -> feet/ankles
- -> abdominal cavity (ascites)
98
cardiac output
volume of blood pumped by each ventricle per minute
99
equation for cardiac output
CO = HR x SV
100
regulation of HR
chronotropic agents
101
positive chronotropic agents
increase HR:
- SNS (NE)
- Epi
- caffeine, nicotine
102
negative chronotropic agents
decrease HR:
- PSNS (Ach)
- PSNS affects only HR not SB
103
average CO
5.25 L/min
104
sympathetic
cardio accelerator center (medulla)
105
parasympathetic
cardio inhibitory venter (medulla)
106
sympathetic atria
increase HR
107
sympathetic ventricles
increases SV
108
vagal tone
holds resting HR lower
109
effect of SNS on HR
increase pacemaker potential (NE opens more Na+ channels)
110
effects of PSNS of HR
decrease pacemaker potential (Ach opens K+ channels)
111
stroke volume
volume of blood ejected by each ventricle per beat
112
regulation of stroke volume
1. preload
2. contractility
3. afterload
113
preload
tension (stretch) in ventricles before contracting = EDV
- increased EDV = increased SV
- increased venous return = increased EDV = increased stretch = increase force of contraction = increased SV
114
contractility
how hard the myocardium contracts for a given preload
- inotropic agents
- increased contractility = increased SV
115
positive inotropic agents
factors that increase Ca+2:
- SNS, NE, Epi
- glucagon (increases cAMP)
- digitalis (increases Ca+2 in cytoplasm)
116
digitalis
used to treat CHF
117
negative inotropic agents
- increased K+ (decreased AP strength) = decreased Ca+2 release
- NOT PSNS --> no input to ventricles
118
afterload
forces ventricles must overcome to pump blood = BP in arteries
- increased BP = decreased SV
- don't want this high
119
ESPVR
end diastolic pressure volume relationship
| - represents max pressure that is developed by left ventricle
120
pressure - volume loop: exercise
1. increase HR = increase HR + increase SV = increase CO = increased BP = increased A2
2. increased SNS = increased contractility (increased Epi) = increased C2 = increased SV2
3. increased skeletal contraction = increased venous return = increased EDV = increased P2 = increased SV2
121
pressure - volume loop: heart failure
- decreased contractility (decreased Ca+2) = increased ESV2 (decreased SV2) --> decreased BP (decreased A2)
122
compensate for heart failure
increased EDV and increased P2, but isn't enough for increased ESV so there is a decreased CO
123
pressure - volume loop: hypertension
increased A2 = decreased SV
to compensate increased SNS = increased HR to maintain CO
--> increased C2
--> P1 doesn't change
124
arteries
away from heart
125
∆P
difference in pressure NOT absolute pressure
| - increased F = increased ∆P
126
where should you measure blood pressure?
on brachial artery with a sphygmomanometer
127
blood pressure
systolic pressure / diastolic pressure
128
average blood pressure
120 mmHg / 75 mmHg
129
pulse pressure (PP)
measure of stress exerted on small arteries by pressure surges generated by the heart
130
pulse pressure equation
PP = systolic - diastolic
131
pulse pressure average
45 mmHg
132
mean arterial pressure (MAP or MABP)
- another measure of stress on blood vessels
| - has most influence on risk of vessels disorders
133
mean arterial pressure equation
MAP = diastolic + PP / 3
134
mean arterial pressure average
90 mmHg
135
hypotension
chronic decrease in blood pressure <90/60 mmHg
136
hypertension
chronic increase in blood pressure >140/90 mmHg
137
during systolic flow, if the artery is not elastic
- allow for very fast flow
| - BP = 380 mmHg
138
during diastolic flow, if the artery is not elastic
- no flow
| - BP = 0 mmHg
139
importance of arterial elasticity
elastic recoil exerts pressure on arteries to keep blood moving during diastole
- decrease pressure fluctuations
- decreased stress on heart and vessels
140
arteriosclerosis
loss of elasticity
| - increase BP with age
141
where is the lowest pressure found?
venae cavae
142
vasodilation
increased radius = decreased resistance = increased flow
| - decreased TPR
143
vasoconstriction
decreased radius = increased resistance = decreased flow
| - increased TPR
144
resistance in vessels
TPR Total peripheral resistance
145
increased SNS on vasomotor tone
increased SNS = increased vasoconstriction = increased TPR
146
decreased SNS on vasomotor tone
decreased SNS = increased vasodilation = decreased TPR
147
vasomotor tone
blood vessels are always somewhat constricted
148
two purposes of vasomotion
1. redirect blood flow
2. ∆ TPR for ∆ BP
- -> increased TPR = increased BP
- -> decreased TPR = decreased BP
149
exercise: blood flow
- brain always gets the same
- increase: muscles, skin, heart
- decrease: kidneys, digestive
150
veins
- low resistance, high compliance
- "capacitance vessels"
- toward the heart
151
venous return is helped by
1. SNS --> vasoconstriction of veins
2. skeletal muscle 'pump'
3. respiratory 'pump;
152
exercise enhances these mechanisms
- increased SNS activity
| - increased venous return = increased EDV (P1) = increased SV = increased CO
153
valve closed during venous return
valve prevents backlog between muscle contractions
154
arrangement of vascular beds
- each tissue gets same quality of blood and can regulate what tissues get blood
- in parallel
155
local control (augoregulation)
ability of tissue to regulate own blood supply
| - increase wastes (increase CO2, increase H+) and decrease O2 = vasodilation
156
neural (rapid / short term) BP control
baroreceptors in carotid sinus and aortic arch = stretch receptors
- send info to cardiac and vasomotor centers in medulla oblongata
- always have tone:
- - increase stretch (increase BP) = increase firing rate
- - decrease stretch (decrease BP) = decrease firing rate
157
hormonal (long term) BP control
via changes in blood pressure and blood volume
158
what is the main form from the renin-angiotensin-aldosterone system
angiotensin II
159
main effects of angiotensin II
1. activates thirst center at hypothalamus, increase ADH
2. widespread vasoconstriction
3. adrenal cortex secrete aldosterone
160
angiotensin II
vasoconstriction (increase TPR), increase ADH, increase aldosterone
- increase BP
161
aldosterone
increase Na+ reabsorption in kidney, water follows Na+ (isotonic)
- increase BV = increase BP
162
antidiuretic hormone (ADH)
increase water reabsorption in kidney
| - increase BV = increase BP
163
atrial natriuretic peptide (ANP)
released from right atrium in response to increased stretch
- decreased aldosterone
- decreased ADH
- decreased Na+ reabsorption in kidney (decreased water)
- vasodilation
- decreased BP
164
primary hypertension
- most common
- unknown cause
- genetic and environmental factors play role
- -> obesity, diet, lack of exercise, smoking
165
secondary hypertension
- kidney damage (increase RAA)
| - endocrine disorder (increase cortisol, increase aldosterone, increase TH)
166
consequences of hypertension
- heart failure --> from hypertrophy = pumping against increased pressure
- atherosclerosis / vascular disease --> MI, stroke, kidney failure
167
treatments of hypertension
goal = decrease cardiac output and/or decrease TPR
- decreased CO
- --> diuretics to decrease BV
- --> beta blockers to decrease HR
- decreased TPR
- --> ACE inhibitors decrease TPR
168
atherosclerosis
artery walls thicken with plaques made of WBC's, cholesterol, and connective tissue
- damage to endothelium = increased inflammation = platelets, WBCs, LDL cholesterol accumulates
169
atherosclerosis consequences
vascular disease
- - coronary artery disease
- - peripheral artery disease
- - stroke / TIA
170
embolism
blood clot (in veins) or plaque fragment traveling through blood stream
