Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A & P I > API_Exam 2 > Flashcards

API_Exam 2 Flashcards

1
Q

what two systems control control contraction and rate

A

intrinsic
extrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are causes of alternans

A

ischemia
myocarditis
digitalis toxicity–purkinje fiber block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what secretes epinephrine and norepinephrine

A

adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

do arterioles need cardiac output to vasoconstrict or vasodilateno

A

no- operate independently, based on tissue need

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does the bainbridge reflex work

A

increased volume in atria signals vmc via vagal afferents to increase heart rate/contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what beat has alternating amplitudes of qrs currents and why

A

electrical alternans-
QRS different heights
incomplete intraventricular block

caused by impulses sometimes being blocked and not passing through the purkinje system

caused by ischemia, myocarditis, a dig toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what makes up the instrinsic system

A

av node
sa node
bundle of his

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what can intrinsic system do in the heart

A

initiate heart beat without any extrinsic impact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why is a heart transplant possible

A

intrinsic system of the heart- automatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what still has to occur in the intrinsic system

A

depolarization and action potential- just doesn’t necessarily need stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the order of the intrinsic flow through the heart

A

sa node-
av node and bundle-
right/left bundle branch-
purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the first structure that takes impulse into ventircles

A

AV bundle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what takes impulse to all parts of the ventricles

A

left and right purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where does SA node sit

A

right atrium, top left back portion near where SVC enters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the SA node made of

A

cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is not found on SA node, internodal pathways, AV node

A

myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why is it significant that sa node, internodal pathways, and av node don’t have myofibrils

A

no contracting abilities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the names of the internodal pathways

A

anterior= most medial
middle= middle pathway
posterior= most lateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why can internodal pathways conduct action potentials very quickly

A

no myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does internodal pathways spread into and what effect does that have

A

spreads into muscles
makes conduction instantaneous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are located between the intercalated disks

A

gap junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the significance of gap junctions

A

lets charge creating action potential to go through easier/quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what structure enables whole atrial/ventricle to contract at same time

A

gap junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what splits off the anterior internodal and goes to the left atrium

A

bachmans bundle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what creates contraction of whole left atrium

A

bachmans bundle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does bachmans bundle cross through to get to left atria

A

interatrial septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

why is it significant that bachmans bundle comes off anterior internodal

A

so left and right atria contract at the same time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what do the internodals come together to form

A

AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is a distention off the av node

A

av bundle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what comes off the av bundle

A

left and right bundle branch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

which ventricle is thicker

A

left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

which ventricle has more bundle branches

A

left
because more muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the left bundle branch responsible for

A

depolarization of intraventricular septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what explains the q wave

A

depolarization of intraventricular septum by left bundle branch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what direction action potential move through interventricular septum

A

upwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what extends off bundle branches

A

purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the flow of action potential through the heart

A

sa node
internodal pathways
av node
av bundle
left/right bundle branch
purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is another name for the av bundle

A

bundle of his

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what muscle is the sa node connected to

A

atrial muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

why does the sa node act as a pacemaker

A

low resting membrane potential
-55- -60

higher intrinsic rate 70-80bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the resting membrane potential of ventricles

A

-90mv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what it the resting membrane potential of atria

A

-55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what causes action potential in atria

A

leaky na channels getting membrane to threshold at -40, then calcium channels open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why is there almost no plateau in atrial contraction

A

potassium channels open but calcium do not like they do in ventricular ap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

why is there no overshoot in atria

A

not as much influx of sodium and calcium at the same time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what kind of leaky channels does atria have and why is that important

A

mostly sodium- causes increased rmp at -55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what causes threshold to be met in atria

A

leaky sodium channels causing mp to hit -40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what happens when mp hits -40 in atria

A

calcium channels open, action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what happens when atrial MP hits 0

A

potassium channels open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is the curve at the top of the atrial action potential

A

Ca channel closing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why doesn’t atria have overshoot in action potential

A

because Na doesnt overflood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

when do leaky sodium channels start having effect during repolarization and what do they prevent

A

-40mv
hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how does sns primarily increase hr

A

increases permeability of sodium and calcium channels so action potentials occur quicker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how does pns primarily decrease hr

A

increases permeability to potassium channels so inside cell is more negative so more calcium/sodium needed to hit threshold, making it harder to get to threshold for action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

why does there need to be a delay in atria contraction and ventricular contraction and what gives the delay

A

time for atrium to put blood in ventricle av node, av bundle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is the delay in the av node, av bundle

A

av node= 0.09 sec
av bundle= 0.04 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

sa node delay

A

0.03

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what tissues acts as insulator so charge stays on pathway and doesn’t go back to atrium

A

atrioventricular fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

av node delay

A

0.09

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

av bundle delay

A

0.04

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what are the two delay periods that occur and what is total time

A

1- until you get to atrioventricular fibrous tissue
2-within av bundle
3- 0.12-0.13 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

time from the two delay periods that occur and what is the total time

A

1- until you get to atrioventriculat fibrous tissue
2- within av bundle
3- 0.12-0.13 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

time from sa node to start of bundle branch

A

0.16 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what causes delay through av node-av bundle

A

less gap junctions- longer for action potential to move

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what structure has many gap junctions

A

purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

why does av bundle have one way conduction

A

atrioventricular fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how long does action potential take to get all the way through the ventricles

A

0.21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what are the normal rates of discharge

A

SA- 70-80/min
AV- 40-60/min
Purkinje fibers 15-40/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

why is the SA node the pacemaker

A

has faster intrinsic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what happens in AV block

A

purkinje fibers pick up pacemaker function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what is the delay in pickup of heartbeat when pacemaker shifts from sa to purkinje in an av block

A

stokes adams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how long does purkinje take to pick up heartbeat in stokes adams syndrome and what happens during this time

A

5-20 seconds
syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what nerve innervates the SA node and AV node junctional fibers

A

PNS (vagal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what neurotransmitter increases potassium permeability and what effect does that have

A

ach- causes hyperpolarization aka decreased rmp leading to decreased heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what neurotransmitter increased sodium/calcium permeability and what effect does that have

A

norepinephrine- more action potentials, more sa node discharge, increased conduction, increased heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is the normal PR interval

A

0.16 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what is the normal QT interval

A

0.35 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what does the p wave represent

A

atrial depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what does the ECG tell you

A

electrical conductivity of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what part of EKG represents delay between atrial/ventricle contraction

A

after p ends and before q
the flat line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what causes spikes on ECG

A

electrical event caused by action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what does qrs represent

A

ventricular depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what does t wave represent

A

ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

why is repolarization of atrium hidden

A

because QRS has greater electrical event so its hidden behind it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

when does ventricular contraction happen on ECG

A

Q to the end of T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what does the p wave immediately precede

A

atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what wave is sometimes not reflected and why

A

q
discharge from intraventricular septum isnt going straight at probe so its not reflected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is the magnitude and direction of action potential

A

vector

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is the axis

A

the summation of magnitude and direction of action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what are the depolarization vs repolarization charges

A

depolarization= positive charge

repolarization= negative charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

where is the ground lead placed

A

right leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what is being read on ECG- electrons impact or direction of electrical charge

A

direction of electrical charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what letters on ECG are negative

A

Q
S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

where on ECG is repolarization moving towards a negative pole

A

T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what letter represents large action potential moving toward apex of heart

A

R wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is a R-R interval time

A

0.83

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

how do you figure heart beat from R-R interval

A

60 seconds/0.83= 72

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

how many chest leads are there

A

6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

which ECG leads are bipolar

A

1 2 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

which leads are augmented (meaning - and 2+)

A

aVR
aVL
aVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what leads give the coronal plane view of the heart?

A

base to apex, anterior surface

bipolar and augmented leads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what leads look at heart from transverse view (cutting heart in half)

A

chest leads (precordial leads)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what precordial leads give view of interventricular septum

A

V1 V2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what precordial leads give anterior view of surface of the heart

A

V3 V4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what precordial leads give view of left ventricle

A

V5 V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

where do you put V4

A

5th intercostal space, mid clavicular line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what does right bundle branch depolarize

A

right ventricular free wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is the direction of magnitude of action potential slightly shifted to the left

A

left ventricle is thicker which shifts axis to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

in what direction does action potential go for depolarization of intraventricular septum

A

left to right

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what charge is repolarization

A

negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what are the phases of action potential through the heart creating axis

A
  1. depolarization of atria- positively charged
  2. delay phase at av node-av bundle 0.12 seconds
  3. AV bundle- depolarization of intraventricular septum initiated by left bundle branch going left to right and superior
  4. depolarization of rest of ventricles (intraventricular septum, left/right ventricular free wall, apex of heart whereaxis is slightly shifted to the left- positive charge)
  5. depolarization moves up ventricular free walls- axis is moving superiorly towards atrium- positive charge
    - all of these yield contraction
  6. repolarization- moving superiorly- negative charge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

measuring direction of flow causes

A

deflection on graph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what are positive/negative direction on ECG

A

positive= up
negative=down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what does ECG measure

A

electrical event- each spike is a different event, qrs is only depolarization of ventricle, t wave is only repolarization of ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

where is apex of heart pointing toward

A

left leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what does lead 1 give view of

A

across top of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

explain direction and charge of bipolar leads

A

1= negative to positive (r to l)
2= negative to positive (r to l downward/diagonal)
3=negative to positive (left side, downward)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

how many positive and negative leads do bipolar have

A

2 neg 1 pos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

how many positive and negative leads do augmented have

A

2 neg 1 positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what are the negative poles in aVF

A

top

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

where are the negative pole in aVR

A

both left side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

where are the negative poles in aVL

A

one side right, one bottom left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what does the last letter tells you in the augmented leads

A

where to put the positive lead
L= left arm
R= right arm
F= left foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what are the angles in augmented leads near the positive pole

A

30 and 30= 60 total

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what view do bipolar and augmented leads give

A

frontal view
aka coronal view

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what lead creates an inverted wave and why

A

avr-
p wave/qrs/t inverted because positive lead is on right arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what determines the wave

A

axis
summation of direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what are chest leads looking at

A

transverse section of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

where do you put V1

A

4th intercostal space, right side of sternum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

where do you put V2

A

4th intercostal space, left side of sternum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

where do you put V4

A

5th intercostal left midclavicular line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

where do you put V3

A

between V2 and V4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

where do you put V5

A

5th intercostal space, left medial axillary line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

where do you put V6

A

5th intercostal space, left midaxiallary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

which leads are in cabreras circle

A

augmented and bipolar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

where does apex of heart point on Cabrera’s circle

A

59 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

which lead points closest to where the apex of the heart points

A

lead 2, 60 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what is in the center of the Cabreras circle

A

heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

why is QRS so big

A

strong summation because of the thickness of the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what is happening during lag time between S and T

A

waiting for repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what lead has smaller r wave and why

A

aVL
depolarization isnt moving directly towards positive pole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what do magnitude of waves depend on

A

direction of axis flow to charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what wave do you plot on cabreras circle to determine significance of axis

A

qrs wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what is a normal axis deviation

A

between -30 to 90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what is it called when axis falls between -30 to -90

A

left axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what is it called when the axis falles within 90 to 180

A

right axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what is it called when axis falls within -180 to -90

A

extreme axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what lead do you look at if lead 1 QRS is positive

A

lead 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what lead do you look at if lead 1 QRS is negative

A

aVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what degrees do you shade if lead 2 has positive QRS

A

-30 to 150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

what degrees do you shade if lead 1 has positive QRS

A

-90 and 90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what degrees do you shade between if aVF is negative

A

0 to -180

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what is the largest axis and therefore the biggest influence

A

ventricular depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

when looking at ECG why is QRS of primary concern

A

represents ventricular depolarization which is the largest axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what is an example of left axis deviation

A

left ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what deviation occurs when lead 1 is negative and aVF is negative

A

extreme axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

what deviation occurs when lead 1 QRS is positive and lead 2 is negative

A

left axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what deviation occurs when lead 1 QRS is negative and aVF is positive

A

right axis deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what are causes of cardiac arrhythmias

A

-abnormal rhythmicity of pacemaker shift from sinus node
-blocks at different points in cardiac impulse
-abnormal pathways of transmission in heart
-spontaneous generation of abnormal impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what happens when SA node is blocked

A

no P waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what does incomplete heart block mean

A

occasions when it is blocked temporarily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what are the incomplete heart blocks

A

first degree AVB
second degree AVB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what is normal PR interval

A

0.16 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

what is a first degree AVB

A

PR interval greater than 0.20 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what does PR interval rarely get above

A

0.45 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

what has PR interval between 0.25-0.45 sec

A

2nd degree heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

what happens in 2nd degree heart block type 1

A

longer longer drop

lengthened PR interval until QRS is dropped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

what happens in second degree type II

A

multiple p waves with QRS, more skipped, more serious

same long PR interval, and dropped QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

what is beating faster in 2nd degree AVB

A

atria faster than ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

what is a total block through the AV node or AV bundle

A

3 degree heart block

complete heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

what block is the p wave completely dissociated from QRST complex

A

3rd degree block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

in what heart block can stokes adams occur

A

3rd degree heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what causes fainting in stokes adams

A

ventricles stop contracting for 5-20 seconds because of overdrive suppression, faints because of poor cerebral blood flow until purkinje kicks in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what is provided for stokes adams patients

A

RV pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

what is happening to SA node in 3rd degree block

A

firing as normal but impulse cannot get through

SO atria beats independently of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

what block is a incomplete interventricular block

A

electrical alternans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

where does electrical alternans occur

A

impulse conduction in peripheral portion of ventricles in purkinje system are blocked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

what happens in electrical alternans

A

impulse is sometimes blocked and sometimes not causing some smaller qrs waves -effects sodium-potassium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

during PACs, what happens to PR interval and P wave

A

shortened, may be inverted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

what happens to impulse in PACs

A

travels from sa node to av node and then back to sinus node causing another discharge before-atrial-filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

what can cause PACs

A

toxins
calcifications
ischemia of nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

what happens to QRS in PVC and why

A

TALL AND PROLONGED because impulse is conduction through slow muscle tissue instead of purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

what happens in the ventricles with PVCs

A

one depolarizes before the other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

what happens to t wave in PVC

A

inverted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

what can cause PVCs

A

cigarettes
coffee
lack of sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

what is long qt syndrome caused by and what can it lead to

A

mutations in Na and potassium channels, torsades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

what does torsades de pointe

A

twisted point

premature depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

what can torsades lead to

A

vfib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

what happens to parts of ventricle during vfib

A

some parts of muscle contract while others are relaxing

no blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

what can overwhelm vfib

A

electrical shock to depolarize ventricle at one time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

why can you live with afib

A

80% of total blood volume from atria to ventricles falls in by gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

what is the most frequent cause of afib

A

atrial enlargement due to AV valve dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

why do cardiac arrests occur

A

hypoxic conditions preventing muscle/conductive fibers from maintaining electrical gradients–DEEP ANESTHESIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

where does blood accumulate in afib and how can you treat it

A

left atrial appendage

remove appendage or watchman (umbrella)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

what heart rate can hypovolemia lead to

A

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

what nerve stimulation can cause bradycardia

A

vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

what can carotid sinus syndrome cause and why

A

bradycardia

sensitive baroreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

what causes sinus arrythmias

A

respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

what is a normal PR interval

A

0.12-0.20 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

in 3rd degree block, why do QRS complexes occur unsynchronized with p waves

A

av node is trying to take over as pacemaker while sa node is also still firing- both are firing independently of each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

what is ventricular escape and when does it occur

A

av node is not stimulated by sa node, before av node starts acting as ectopic pacemaker, there is no ventricle contracting because of no signal so syncope occurs and then av node kicks in- stokes adams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

what can cause and is associated with electrical alternans

A

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

what is a pulse deficit

A

ventricles cannot fill during PAC/PVC so stroke volume is decreased/absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

what is missing from ecg or occurs after qrs during av node premature contraction

A

p wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

where does impulse originate during AV node PVC

A

AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

what are 3 characteristics of PVC

A

1- qrs is considerably prolonged (impulse is through slow muscle rather than purkinje)
2- qrs complex is high
3- inverted t wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

what is another name for long QT syndrome and what causes it

A

torsades de pointes- premature depolarization- can lead to death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

what is it called when ventricle does not repolarize well because of tissue death and causes ST elevation

A

STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

what are inverted T waves indicative of

A

ischemia, most commonly caused from MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

why do MIs usually impact T wave

A

tissues will not repolarize as well because of ischemia or necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

how much blood is in pulmonary circulation

A

9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

how much blood is in heart

A

7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

how much blood is in arteries

A

13%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

how much blood is in arterioles and capillaries

A

7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

what are major functions of circulatory system

A

transport nutrients to tissues
transports waste away from tissue
transport hormones tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

difference between endocrine vs exocrine

A

endocrine= gets in blood
exocrine=impacts neighboring cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

how much blood does veins, venules, and venous sinuses have

A

64%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

where is body reservoir of blood

A

veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

what transports blood through high pressure side to get to capillaries

A

arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

average heart chamber pressures

A

ra= 5
rv= 24
la= 8
lv=130
aorta= 120/80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

what side of the heart is the high pressure side

A

left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

how do arterioles control blood flow

A

constrict or dilate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

what vascular structure is a major contributor to regulation of BP

A

arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

where is the site of water and solute exchange between vessels and tissues

A

capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

what component of circulation has largest total surface area

A

capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

what part of vasculature has highest velocity

A

aorta > arterioles > small veins > capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

why does pressure decrease in capillaries, venules, veins

A

because there are so many more of them
large fire hose being connected to 3 smaller= decreased pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

why is venous pressure so low

A

veins are distendable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

what is blood flow controlled by

A

tissue needs
exercise=increase tissue needs=increased HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

what is controlled independent of local blood flow or cardiac output control

A

arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

what is controlled by local tissue flow

A

cardiac output

more need=more cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

what 4 ways is arterial pressure controlled by

A

1- increased force of heart pump
2- contraction of large veins
3. generalized constriction of arterioles
4. long term renin made by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

what do arterioles do when tissue needs more blood flow/less blood flow

A

dilates- irrespective of co and blood flow

constricts- also irrespective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

what do walls of blood vessels create

A

resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

because of resistance how does this effect shape of blood flow through vessel

A

parabolic- arched, blood closest to walls is slower than blood in middle of vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

what does aortic valve stenosis do and how does it impact flow

A

increases resistance, decreases flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

what kind of flow is a bruit

A

turbulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

what can bruit aka turbulent flow cause

A

damage to intima (inside) vessel, which fills with cholesterol creating plaques creating clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

what organs have the most flow by percent (top 3)

A

liver
kidney
brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

what is flow through a blood vessel determined by

A

pressure difference/resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

what are some causes of turbulent flow

A

high velocity
sharp turn
rough surfaces
rapid narrowing of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

what does turbulent flow tend to cause

A

murmurs or bruits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

what does turbulent flow increase

A

wall stress on vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

what is measure of blood flow through a vessel for given pressure difference

A

conductance
larger conductance=smaller resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

does resistance increase or decrease in capillaries

A

increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

how does change in hematocrit/viscosity change blood flow

A

increased viscosity= decreased flow (polycythemia)

decreased viscosity=increased flow (anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

what is distendability

A

ability to stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

what is compliance

A

pressure needed to make stretch increased compliance=decreased pressure needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

what is capacitance

A

volume to cause stretch (capacity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

how many times more distend able are veins than arteries

A

8x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

what kind of muscle is in the artery and where

A

smooth muscle in media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

why can veins not contract as much as artery

A

smaller, less defined media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

why isnt artery as distendable as vein

A

more defined media

253
Q

what does artery being less distendable cause

A

higher pressure

254
Q

what is vascular capacitance

A

the total blood that can be stored in given portion of circulation

255
Q

how much more capacitance do veins have than arteries

A

24x

veins hold more blood in circulation

256
Q

what happens to cardiac output when veins contract

A

increased volume to heart

257
Q

what is only system that has impact on circulation and heart

A

SNS

258
Q

what system only has impact on the heart

A

PNS

259
Q

what is tone

A

constant degree of SNS stimulation in circulation

260
Q

how do you cause dilation in vessels

A

inhibit SNS

261
Q

formula for pulse pressure

A

systolic-diastolic

262
Q

why does pressure and therefore speed have to fall in capillaries

A

to give time for nutrient/co2 exchange

263
Q

factors that affect pulse pressure

A

stroke volume
arterial compliance-inverse peripheral resistance
cardiac output

264
Q

what increases pulse pressure

A

arteriosclerosis
PDA
aortic regurg

265
Q

what can decrease pulse pressure

A

aortic stenosis

266
Q

how does PDA increase pulse pressure

A

shoots blood into aorta from pulmonary artery which increases volume increasing systolic

267
Q

how does aortic regurg increase pulse pressure

A

aortic valve doesn’t close all the way, blood leaks back into left ventricle

268
Q

how does aortic stenosis decrease pulse pressure

A

valve opening is smaller reducing flow of blood

269
Q

what is pressure in superior sagittal sinus

A

-10mmhg

270
Q

what keeps blood from pooling in legs

A

valves

271
Q

why do varicose veins occur

A

+90 pressure is building against valve until it folds in and fluid pools in veins- comes from standing

272
Q

factors that increase right atrial pressure

A

increased blood volume
increased venous tone
dilation of arterioles
decreased cardiac function

273
Q

what are the needs of tissues

A

delivery of oxygen, glucose, amino acids
removal of carbon dioxide/hydrogen/waste
transport hormones

274
Q

what 3 factors/systems control blood flow

A

1- tissue demand
2- neurological system (short term)
3- hormones (long term)

275
Q

when you have an immediate need for blood flow/pressure adjustment, what responds

A

neurological system (short term)

276
Q

what makes long lasting changes in blood pressure in 1-3 days

A

hormones (renin)
increased number of vessels
size of vessels

277
Q

what is the growth of new blood vessels

A

angiogenesis

278
Q

what causes angiogenesis

A

increased oxygen demand for sustained period of time
scar, tumor

279
Q

what is it called when vessels stop growing in retina when premature baby is in o2 chamber, then overgrow once taken out of o2 chamber and cause blindness

A

retrolental fibroplasia- can cause blindness

280
Q

what causes angiogenesis

A

ischemic tissue
rapidly growing tissue (tumors)
tissue with high metabolic rates

281
Q

what vasoconstrictors control blood flow

A

norepinephrine and epi
angiotensin II (always vasoconstrict)
vasopressin
Endothelin

282
Q

what vasodilators control blood flow

A

bradykinin
serotonin
histamine
prostaglandins
nitric oxide

283
Q

what does norepi always do

A

vasoconstrict

284
Q

what can epi do that norepi cannot

A

vasodilate

285
Q

what does the alpha 1 receptor do

A

vasoconstriction

286
Q

what does beta 1 receptor do

A

increase heart rate

287
Q

beta 2 action

A

dilates vessels and airway

288
Q

what does epinephrine do to coronary arteries

A

vasodilation

targets beta 2 receptors

289
Q

what is endothelin

A

inside all vessels and when it gets traumatized causes vasoconstriction

290
Q

what is a very potent vasoconstrictor

A

vasopressin

291
Q

what causes vasodilation to get blood and neutrophils to tissue

A

bradykinin,
histamine,
prostaglandin

292
Q

how does nitric oxide affect rbc’s

A

helps make oxygen more soluble to get out of RBC and into tissue

293
Q

how does nervous system regulate circulation

A

redistribute blood flow
increasing pumping activity of heart
rapid control of arterial pressure
regulates via ans

294
Q

where are baroreceptors found

A

carotid sinus
aortic arch
right atria

295
Q

does PNS cause vasodilation

A

NO

it inhibits the SNS system

296
Q

what PNS nerve slows down heart rate

A

vagus nerve

297
Q

does SNS increase contractility of heart

A

YES

298
Q

what structures vasoconstrict and vasodilate

A

arterioles

299
Q

why do capillaries not constrict

A

velocity of blood needs to be low for nutrient exchange

300
Q

what stimulates the large veins and the heart

A

SNS

301
Q

where are SNS vasoconstrictor effects of fibers less potent

A

cerebral and coronary

302
Q

where are there more vasoconstrictor fibers

A

kidney
gut
spleen
skin

303
Q

what increases with increased venous constriction

A

cardiac output= increased preload

304
Q

where is VMC located

A

medulla(reticular)
lower 1/3 of pons

305
Q

what is the VMC composed of

A

vasoconstrictor area
vasodilator area
sensory area

306
Q

what stimulated vasomotor tone

A

vasocontrictor area of VMC
continuously transmits signals

307
Q

what part of VMC causes increased heart rate and contractility

A

lateral portions

308
Q

what can cause excitatory/inhibitory effects on VMC

A

hypothalamus

309
Q

what part of VMC transmits signals via vagus nerve to heart and what does this signal do

A

medial

decreases heart rate

310
Q

what vessel can epi dilate and with what receptor

A

coronary artery

beta 2

311
Q

what happens in vasovagal syncope

A

excitement/stress: stimulates blood vessels to dilate and-vagalcenter-signals-decrease-in-heart-rate= no blood flow to brain= syncope

312
Q

what is increased/decreased SVR

A

constriction or dilation of peripheral vessels

313
Q

how does VMC increase arterial pressure

A

-constrict arterioles of body to increase svr
-constrict large vessels to increase venous return/cardiac output
-direct increase of co by increasing hr and contractility

314
Q

what occurs with arterial constriction

A

venous constriction to keep blood at level cardiac output

315
Q

nervous system control of arterial pressure

A

exercise-> vmc-> increase sns/decrease pns-> increased svr/venous return/hr/heart strength= increased arterial pressure

316
Q

what are baroreceptors important in

A

short term regulation of arterial pressure

317
Q

what are baroreceptors sensitive to

A

stretch
changes in pressure

318
Q

what nerves do baroreceptors send messages through in carotid artery

A

hering nerve to glossopharyngeal nerve to vmc

319
Q

what nerves do baroreceptors utilize to regulate blood pressure in aortic arch

A

vagus nerve

320
Q

what are carotid bodies sensitive to

A

chemicals aka chemoreceptors

321
Q

do baroreceptors or carotid bodies drive BP

A

baroreceptors

322
Q

when is baroreceptor reflex most sensitive

A

100mmhg

323
Q

when do carotid baroreceptors respond to change in pressure

A

60-180 mmhg

324
Q

pressure increases, so the number of impulses from carotid sinus baroreceptors increases leading to:

A

inhibition of vasoconstrictor activation of vagal center

325
Q

how do we maintain consistency in blood pressure

A

baroreceptors

326
Q

where are carotid bodies found

A

carotid bifurcation and aortic arch

327
Q

what chemicals do chemorecptors sense

A

lack of O2
CO2 excess
H+ excess

328
Q

can you see carotid bodies

A

NO

329
Q

at what pressure are chemoreceptors stimulated and what does it do when stimulated

A

below 80mmhg

stimulates VMC

330
Q

what is the flow of chemoreceptors in carotid bodies

A

decreased oxygen, increased co2, low ph->chemoreceptors–>vmc–>increase sns= increase bp/resp rate

331
Q

when is CNS ischemic response activated

A

cerebral ischemia

332
Q

what is one of the most powerful activators of sympathetic vasoconstricor

A

CNS ischemic response

333
Q

what triggers CNS ischemic response

A

reduced blood flow causes increased co2 which stimulates vmc to increase art pressure

334
Q

when is cns ischemic response triggered

A

60mmhg

greatest at 15-20 mmhg

335
Q

what happens in the cushing reaction in cns ischemic resonse

A

csf pressure increases–>collapses brain vessels–>sns reponse–>increased bp/hr to open up vessels in brain

336
Q

what is activated when venous return increases to right atrium and therefore sa node

A

baroreceptor response from stretch- increases heart rate to pump blood out

337
Q

what nerve does the baroreceptors in the right atria transfer signals to brain

A

vagus afferents (not really on vagus, hitches a ride)

338
Q

How does atrial natriuretic peptide work?

A

released by overstretched heart cells in right atria
stimulates kidney to excrete sodium and therefore water

339
Q

what are the ways right atria contributes to bp regulation

A

1- baroreceptors- sense stretch
2- anp- stimulates increased na/water excretion
3-decreases renal flow/actvity-increased na/water excretion
4-bainbridge reflex- senses pressure, afferents, vmc, increase hr/contractility

340
Q

what happens to GFR with vasoconstriction

A

decreases

341
Q

what prevents damming of blood in veins, atria, ventricle, and pulmonary circulation

A

bainbridge reflex

342
Q

what is the bainbridge reflex

A

when atrial pressure increases, heart rate increases

343
Q

what are short and long term regulations of increased atrial pressure

A

long term= atrial natriuretic peptide

short term=bainbridge reflex

344
Q

how long do kidneys take to impact pressure control

A

24-72 hours

345
Q

when arterial pressure/ecfv increases, how do kidneys react

A

increased sodium excretion

346
Q

how much of the body is water

A

60%

347
Q

what is difference between natriuresis and diuresis

A

nat=get rid of na and water

diuresis=get rid of water

348
Q

do changes in svr affect long term arterial pressure

A

no- kidneys will respond before then

349
Q

how does ecfv (extracellular fluid volume) increase affect svr graph

A

decreases at first to make room, then increases

350
Q

what is autoregulation in capillary

A

slows down blood (increase peripheral resistance) to let exchange of nutrients happen even with increased cardiac output

351
Q

bp vs blood flow

A

pressure increases with decreased radius= bp, constriction

blood flow= decreases with decreased radius

352
Q

what controls cardiac output

A

heart rate
contraction
preload
afterload

353
Q

what happens to resistance in aortic stenosis

A

increased resistance, decreased cardiac output, increased blood pressure due to calcium build up

354
Q

what happens when you try to push same volume of fluid through a smaller hole than normal

A

increased pressure

355
Q

what is it called when blood builds up in ventricles because of aortic stenosis

A

increased afterload

356
Q

how do you increase/decrease afterload

A

vasoconstrictors/vasodilations

357
Q

what makes angiotensinogen and how often

A

liver

makes it all the time

358
Q

what produces renin and when

A

kidney- decrease in bp or ecf (really senses decreased gfr)
increased urine na+

359
Q

what can angiotensinogen do by itself

A

nothing

360
Q

what makes angiotensin 1

A

angiotensinogen and renin

361
Q

where is angiotensin converting enzyme produced and when

A

lungs (alveoli)- produced all the time

362
Q

where in kidney is renin produced

A

juxtaglomerular cells

363
Q

what does angiotensin 1 do by itself

A

nothing

364
Q

how is angiotensin II made

A

angiotensin 1 + ace

365
Q

what is GFR

A

pressure required to push blood through kidney

366
Q

what are the two roles of angiotensin II

A

1- potent vasoconstrictor by itself
2- stimulates release of aldosterone from adrenal cortex which tells kidney to save sodium and thus water increasing blood volume and bp

367
Q

what is the only thing more potent than angiotensin II

A

vasopressin aka adh

368
Q

where is aldosterone released from and what stimulates its release

A

adrenal cortex- angiotensin II

369
Q

what is most common se of ace inhibitor

A

cough- since it is produced by lungs

370
Q

what does ace inhibitor do

A

inhibits binding of ace- so ace is still made and builds up in lungs causing cough

371
Q

what happens to sodium on ace inhibitors

A

more excreted through urine since aldosterone isn’t released to stimulate sodium retention

372
Q

how do arb’s work and what does it not have

A

angiotensin II receptor blocker- cough side effect

373
Q

why is using the raas system to control blood pressure preferable

A

not directly affecting heart so patient can still have good activity levels

374
Q

what system is important in maintaining normal arterial pressure during changes in na intake

A

raas

375
Q

what do renin levels fall to when sodium intake is increased

A

near 0

376
Q

when do renin levels increase in relation to Na intake

A

renin increases when sodium intake decreases

377
Q

what factors decrease renal excretion and increase bp

A

1- angiontensin II
2- aldosterone
3- sns activity (vasoconstriction=decreased blood flow)
4-endothelin

378
Q

what kind of receptors do skeletal muscles have to get more blood flow

A

beta 2- so vessels dilate to get more blood flow to them

379
Q

when you exercise, your heart rate increases so you need more blood, where does it come from and how

A

venous system- vasoconstriction of veins

380
Q

what factors increase renal excretion and reduce bp

A

1- atrial natriuretic peptide (excess volume in atria triggers sodium excretion in kidney)
2- nitric oxide
3- dopamine

381
Q

what drives cardiac output and pressure

A

tissue demand/metabolic needs

382
Q

what is prehypertension

A

120-139/80-89

383
Q

what is hypertension

A

greater than 140/90

384
Q

what is stage 1 hypertension

A

140-159/90-99

385
Q

what is stage 2 hypertension

A

160 or greater/100 or greater

386
Q

what can increased bp for long periods do to kidneys

A

decreases filtering ability of kidney

387
Q

what are ischemic vs hemorrhagic strokes

A

ischemic= blockage, clot
hemorrhagic- broken vessel, blood leaks out

388
Q

how many hypertensive patients have primary hypertension and what causes it

A

90% unknown

389
Q

how many people with primary hypertension are overweight

A

2/3

390
Q

meds for HTN

A

ace inhibitors
arbs
diuretics
beta blockers
ccb

391
Q

what anti htn meds do you want to start with

A

least amount and most natural and then progress to beta blockers and ccb

392
Q

what determines cardiac output

A

muscle mass/tissue mass-
peds have increased tissue needs so they have increased hr to increase co

393
Q

when happens to co as you get older

A

lose muscle mass= cardiac output needs decrease

394
Q

does peripheral circulation or heart control cardiac output

A

peripheral circulation

395
Q

what is cardiac output proportional to

A

tissue oxygen use/demand
svr

396
Q

what does increased right atrial pressure cause in venous system

A

decreased venous return

397
Q

when does right atria decrease venous return

A

when right atrial pressure is higher than veins coming to it
so higher right atrial pressure=lower venous pressure

398
Q

when volume of blood is increased in right atrium, what happens to cardiac output

A

increases

399
Q

what happens to cause cardiac output graph to be hypoeffective

A

decreased heart ability to pump

stenosis,

valvular disease,

tamponade

400
Q

what happens to cause cardiac output graph to be hypereffective

A

1- increase sns/decrease pns
2-hypertrophy (pumps harder, more often)

401
Q

does hypertrophy of heart have to be pathological

A

no can be in healthy people that exercise a lot

402
Q

how does aortic stenosis affect cardiac output

A

decrease it

403
Q

what causes normal sinus arrythmias

A

breathing

404
Q

what happens to intrapleural pressure during breathing

A

inhale= increases pressure
exhale=decreases pressure

405
Q

how does copd affect heart

A

increased pressure in lungs decreases cardiac output

406
Q

how does ipp above 0 affect heart

A

increase pressure on right atria

407
Q

what is fluid collecting in pericardial sac that increases pressure on heart

A

tamponade- atria/ventricle cannot fill with blood

408
Q

how would blowing out on trumpet affect cardiac output

A

decreased cardiac output because of increased pressure

409
Q

what is the pressure in the system when heart isn’t pumping or pressure required to fill the system

A

mean systemic filling pressure

410
Q

what is normal MSFP

A

7

411
Q

when right atrial pressure is low, venous return is high, as right atrial pressure increases due to venous return, venous return decreases. When does venous return stop decreasing

A

msfp of 7 mmhg
equilibration of venous return and right atrial pressure

412
Q

when right atrial press increases….

A

venous return decreases

413
Q

how does right atria influence cardiac output

A

amount dumped into right atria from veins determines cardiac output- first portion of co

414
Q

what happens to msfp when right atria resistance is increased/decreased

A

decreased/increased- inverse

415
Q

if sns is decreased what impact does it have on veins

A

increases venous compliance

416
Q

what does spinal anesthesia do to sympathetic chain ganglion

A

suppresses them, so decreases sns response, decreases cardiac output

417
Q

what is long term blood pressure balancing system

A

kidneys- raas

418
Q

what is short term blood pressure balancing system

A

neurological system

419
Q

how many ml’s go out of left ventricle per beat

A

72cc’s- stroke volume

420
Q

what is stroke volume equation

A

Esv-edv
normal= 120-50= 70
70/120=58%= ejection fraction

421
Q

what is volume left in ventricle after contraction and what happens when it is increased

A

afterload- decreased cardiac output

422
Q

what does pns do to heart rate

A

decrease heart rate

423
Q

what happens to co when right atrial pressure increases

A

increases- atria is pushing more blood through

424
Q

when does venous return happen to right atria

A

diastolic phase

425
Q

when right atrial pressure decreases, when happens to venous return

A

increases
i.e. during diastolic phase, right atrial pressure decreases because it pumps out all of it’s blood, so venous fills it

426
Q

what happens to increase or decrease venous return

A

increase= venous constriction
decrease= blood loss

427
Q

what is msfp

A

pressure required to bring venous return to 0

428
Q

what are some causes of tachycardia

A

(1) exercise
(2) increased body temperature
(3) sympathetic stimulation (such as from loss of blood and the reflex stimulation of the heart),
(4) toxic conditions of the heart.

429
Q

what is bradycardia

A

means a slow heart rate usually less than 60 beats/min.

Ex: athletes who have a large stroke volume, excessive vagal stimulation (e.g., carotid sinus syndrome)

430
Q

Impulses through A-V node and A-V bundle (bundle of His) are slowed down or blocked due to

A

-ischemia of A-V nodal or A-V bundle fibers (can be caused by coronary ischemia).
-compression of A-V bundle (by scarred or calcified tissue).
-A-V nodal or A-V bundle inflammation.
-excessive vagal stimulation.
-excess digitalis.

431
Q

characteristics of complete heart block

A

-Total block through the A-V node or A-V bundle
-P waves are completely dissociated from QRS-T complexes.
-Ventricles escape and A-V nodal rhythm ensues.

432
Q

characterstics of first degree heart block

A

-Normal P-R interval is 0.16 sec.
-If P-R interval is >0.20 sec, first-degree block is present (but P-R interval seldom increases above 0.35–0.45 sec).

433
Q

characteristics of 2nd degree heart block

A

-P-R interval increases to 0.25–0.45 sec.
-Some impulses pass through the A-V node and some do not thus causing “dropped beats.”
–Second-degree Mobitz Type I (Wenckebach)—has increasing P-R interval then a dropped beat.
–Second-degree Mobitz Type II—has fixed long P-R interval then a dropped beat
-Atria beat faster than ventricles.

434
Q

characteristics of stokes adams syndrome

A

-Complete A-V block comes and goes.
-Ventricles stop contracting for 5–30 sec because of overdrive suppression meaning they are used to atrial drive.
-Patient faints because of poor cerebral blood flow.
-Then, ventricular escape occurs with A-V nodal or A-V bundle rhythm (15–40 beats/min).
-Pacemakers are needed for these patients.

435
Q

incomplete intraventricular block (electrical alternans)

A

-Impulse is sometimes blocked and sometimes not in peripheral portions of Purkinje system resulting in abnormal QRS waves.
-Can be caused by ischemia, myocarditis, and digitalis toxicity

436
Q

PAC characteristics

A

-P-R interval is shortened if ectopic foci originating the beat are near the A-V node.
-The impulse travels through the A-V node and back toward the sinus node causing discharge of the sinus node.
-Next sinus discharge will thus be late.
-An early contraction does not allow heart to fill with blood causing a low stroke volume and a weak radial pulse.

437
Q

PVC characterstics

A

-QRS is prolonged because impulse is conducted through muscle which has slow conduction.
-QRS voltage is high because one side depolarizes ahead of the other.
-P is absent. QRS is wider and taller. T shows opposing polarity to QRS.

438
Q

characteristics of atrial paroxysmal tachycardia

A

-Paroxysmal means a series of rapid heartbeats suddenly start and then suddenly stop.
-Can be stopped with a vagal reflex or drugs
-P wave is inverted if origin is near A-V node.
-Occurs by re-entrant pathways

439
Q

what can ventricular paroxysmal tachycardia lead to

A

vfib or vtach

440
Q

what are causes rentry vfib

A

-Pathway around the circle is too long (e.g., dilated heart)
-Velocity of conduction is decreased (block, ischemia, high potassium)
-Refractory period is shortened (sympathomimetics, ischemia)

441
Q

characteristics of vfib defibrillation

A

1000 volts direct current is applied for a few milliseconds.

All parts of the heart become refractory and remain quiescent for 3–5 seconds until new pacemaker is established.

If used later than one minute after fibrillation, the heart is too weak to defibrillate and may have to be hand-pumped.

442
Q

how does afib effect the heart efficiency

A

efficiency is decreased by 20-30%

443
Q

characteristics of a flutter

A

-Single large impulse wave travels around atria in one direction
-Atria contracts at 200–350 beats/min.
-A-V node will not pass signal until 0.35 sec elapses after the previous signal.
-Therefore, atria may beat 2 or 3 times as rapidly as the ventricle.

444
Q

characteristics of cardiac arrest

A

-Usually occurs due to hypoxic conditions in the heart which prevents muscle and conductive fibers from maintaining their electrolyte gradients
-Unconsciousness after 4–5 seconds
-Fatal after 1–3 minutes if ventricular fibrillation or asystole is not reversed.
-Brain damage if circulatory arrest prolongs over 5 minutes

445
Q

describe vectorial analysis of ecg

A

-The current in the heart flows from the area of depolarization to the polarized areas (from − to +).

-The electrical potential generated can be represented by a vector, with the arrowhead pointing in the positive direction.

The length of the vector is proportional to the voltage of the potential.

The generated potential at any instance can be represented by an instantaneous mean vector.

The normal mean QRS vector is about 59 degrees.

446
Q

draw lead angles

A
447
Q

why is axis of lead I zero degrees

A

because the electrodes lie in the horizontal direction on each of the arms

448
Q

why is axis lead II +60 degrees

A

because the right arm connects to the torso in the top right corner, and left leg connects to the torso in the bottom left corner.

449
Q

what is the axis lead III

A

120 degrees.

450
Q

what is the axis of aVR

A

210 degrees

451
Q

what is axis of aVL

A

-30 degrees

452
Q

what is axis of aVF

A

90 degrees

453
Q

where should p wave be positive

A

Begins at sinus node and spreads toward A-V node.

This should give a + vector in leads I, II, and III.

454
Q

characteristics of ventricular repolarization

A

First area to repolarize is near the apex of the heart.

Last areas, in general, to depolarize are the first to repolarize.

Septum and Endocardium: first to depolarize—last to repolarize—longer contraction

Outer surface of ventricles: last to depolarize—first to repolarize

Repolarized areas will have a + charge first; therefore, a + net vector occurs and a positive T wave.

455
Q

why can you not see atrial t wave

A

Cannot be seen because of QRS complex.

Atrial depolarization is slower than in ventricles, so first area to depolarize is also the first to repolarize, giving a negative wave in leads I, II, and III.

456
Q

what can cause left axis deviation

A

Changes in heart position: left shift caused by expiration, lying down, and excess abdominal fat.

Hypertrophy of left ventricle (left axis shift) caused by hypertension, aortic stenosis, or aortic regurgitation causes slightly prolonged QRS and high voltage.

457
Q

what can cause right electrical axis deviation

A

Hypertrophy of right ventricle (right axis shift) is caused by
pulmonary hypertension,
pulmonary valve stenosis, and
interventricular septal defect.

All cause slightly prolonged QRS and high voltage.

458
Q

characteristics of LBBB

A

QRS is prolonged (> 0.12 sec).

Lead V1 has a wide negative S wave’.

Lead V6 has a “rabbit ear” pattern.

459
Q

characteristics of RBBB

A

QRS is prolonged (> 0.12 sec).

Lead V1 has a positive secondary R wave.

Lead V6 has a slurred terminal S wave.

460
Q

what can cause increased voltages in bipolar limb leads

A

Most often caused by increased ventricular muscle mass
(e.g., hypertension, marathon runner, aortic or pulmonary valve stenosis).

461
Q

characteristics of decreased voltage limb leads

A

Cardiac muscle abnormalities (old infarcts causing decreased muscle mass, low voltage EKG, and prolonged QRS).

Conditions surrounding heart (fluid in pericardium, pleural effusions, emphysema).

Anterior–posterior rotation of apex of heart.

462
Q

what is usually the cause if the QRS > 0.12 seconds

A

usually a conduction block

462
Q

what is the usual cause of prolonged QRS

A

caused by delayed conduction of cardiac impulse through ventricles

One cause is cardiac hypertrophy.
One cause is a Purkinje system block.

463
Q

what can unusual QRS be caused by

A

local conduction blocks which may cause multiple QRS peaks.

464
Q

what kind of charge does injured muscle emit

A

negative charges throughout each heartbeat

465
Q

describe current of injury

A

Damaged cardiac muscle remains partially or totally depolarized all the time (goes from injured—negative end—to healthy area)

466
Q

what are some causes of current of injury

A

(1) local ischemia,
(2) mechanical trauma,
(3) infection.

467
Q

what indicated an anterior lesion infarct

A

If the current of injury in the chest lead is negative, the chest lead is in an area of negative potential which indicates an anterior lesion.

468
Q

what indicated a posterior lesion infarct

A

If the current of injury in the chest lead is positive, the chest lead is in an area of positive potential which indicates a posterior lesion.

Bipolar and augmented unipolar leads help to further determine the injured area of the heart.

469
Q

when would a Q wave develop

A

A Q wave may develop and represent the “scar” on myocardial muscle after infarction.

The lead/leads that show the Q wave help to identify the location of the scar.

470
Q

T wave abnormalities of

A

Ventricular repolarization usually occurs in the opposite direction as depolarization which causes an upright T wave in the three standard leads.

Prolongation of repolarization may change the T wave axis and morphology (flattened, taller, biphasic, inverted).

Examples: Right or left bundle branch blocks, ischemia, digitalis toxicity, changes in K+.

471
Q

how does SA node act as a pacemaker

A

Acts as pacemaker because membrane leaks Na+ and membrane potential is −55 to −60mV.

The constant leak of Na+ makes resting potential to gradually rise

472
Q

when are fast Na channels inactivated

A

at -55mv

473
Q

when do slow Na Ca channels open causing an action potential

A

-40mv

474
Q

when do Ca channels close and K channels open more

A

after 100-150msec

helps return membrane potential to -55mv

475
Q

which internodal pathway carries impulses to left atrium

A

anterior interatrial band

476
Q

what is the action of the AV node

A

Delays cardiac impulse

Delay A-V node—0.09 sec.
Delay A-V bundle—0.04 sec.

477
Q

what is the transmission time between AV bundles and last of ventricular fibers

A

0.06 sec (QRS time)

478
Q

what is the only conducting path between atria and ventricles

A

AV node and left/right AV bundles

479
Q

characteristics of purkinje system

A

Fibers lead from A-V node through A-V bundle into ventricles.

Fast conduction; many gap junctions at intercalated disks

480
Q

describe cardiac impulse timing

A
481
Q

what is ectopic pacemaker

A

A portion of the heart with a more rapid discharge that surpasses the sinus node

Also occurs when transmission from sinus node through the A-V node is blocked (A-V block).

Sinus node discharge does not get through, and next fastest area of discharge becomes pacemaker of the heart.

New pacemaker is in AV node or penetrating part of AV bundle.

If that region fails, Purkinje fibers take the lead (but at lower rate).

482
Q

where does PNS nerves innervate

A

SA node and AV junctional fibers proximal to AV node

483
Q

what is PNS effects on heart

A

Acetylcholine decreases SN discharge and excitability of A-V fibers, slowing the heart rate.

Cause hyperpolarization because of increased K+ permeability in response to acetylcholine (increased negativity inside)

This causes decreased transmission of impulses maybe temporarily stopping heart rate.

Ventricular escape occurs.

484
Q

SNS nerves effect on heart rate

A

Releases norepinephrine at sympathetic ending

Causes increased sinus node discharge

Increases rate of conduction of impulse

Increases force of contraction in atria and ventricles

485
Q

how does norepinephrine effect heart

A

Norepinephrine increases permeability to Na+ and Ca+, causing a more + resting potential, accelerating self-excitation, and excitability of AV fibers.

486
Q

what is a normal QT interval

A

0.36 sec

(0.36–0.40, QTc ≤ 0.46) and is the duration of time from the beginning of the Q wave to the end of the T wave

487
Q

where does ventricular depolarization start

A

at the ventricular septum and the endocardial surfaces of the heart

488
Q

describe lead I - and + terminals

A

The negative terminal of the EKG is connected to the right arm,

the positive terminal is connected to the left arm.

489
Q

describe lead II - and + terminals

A

The negative terminal of the EKG is connected to the right arm,

the positive terminal is connected to the left leg.

490
Q

describe lead III - and + terminals

A

The negative terminal of the EKG is connected to the left arm,

the positive terminal is connected to the left leg.

491
Q

what is Einthovens Law

A

the electrical potential of any limb equals the sum of the other two (+ and − signs of leads must be observed).

If Lead I = 0.5 mV
and Lead III = 0.7 mV

Lead II = 0.5 + 0.7 = 1.2 mV.

492
Q

positive lead flow going toward negative lead=

A

negative deflection on ECG

493
Q

negative lead flow going toward positive lead =

A

positive reading on ECG

494
Q

a negative pole flow going towards a negative pole =

A

positive reading on ECG

495
Q

what leads look at the interventricular septum on ECG

A

V1 and V2

496
Q

what leads give you frontal view of the heart

A

V3 and V4

497
Q

what leads give you a left side view of the heart

A

V5 and V6

498
Q

what are the major functions of the circulatory system

A

-transporting nutrients to the tissues
-transporting waste products away from the tissues
-transporting hormones

499
Q

what are the two circulatory systems

A

pulmonary circulation
systemic circulation

500
Q

what is the function of arteries

A

transports blood to tissues under high pressure (100mmHg)

501
Q

what is the function of arterioles

A

-control site for blood flow
-major site of resistance in circulation

502
Q

what is the function of capillaries

A

major site of water and solute exchange between blood and tissues

503
Q

what is the function of large veins and venules

A

returns blood to the heart under low pressure

serves as s reservoir of blood

504
Q

what is the function of pulmonary circulation

A

site of oxygen and carbon dioxide exchange

505
Q

what is the largest component of circulation (vessel wise)

A

capillaries

506
Q

what is the purpose of capillaries

A

allow for reduced pressure and velocity to allow for gas and nutrient exchange

507
Q

define velocity

A

blood flow is the speed at which blood flows in the circulation

velocity of blood flow= blood flow/ cross-sectional area

508
Q

what happens when blood pressure falls

A
  1. increase force of heart pumping/ contracting
  2. contraction of large venous reservoirs (SNS controlled)
  3. cause generalized constriction of arterioles (SNS)
  4. LONG TERM (hours to days) Renin produced by kidneys (RAAS)
509
Q

what is blood flow

A

the quantity of blood that passes a given point in the circulation in a given period of time

510
Q

flow through a blood vessel is determined by

A
  1. pressure difference between two ends of the vessel
  2. resistance of the vessel
511
Q

what can increased velocity cause

A

turbulence and bruits

512
Q

what is blood pressure

A

the force exerted by the blood against any unit area of vessel wall

513
Q

what is resistance in the blood vessels

A

it is the impediment to blood flow in a vessel

514
Q

what is conductance

A

a measure of the blood flow through a vessel for a given pressure difference

mL/min per mmHg

515
Q

equation for conductance

A

conductance=1/ resistance

516
Q

what is conductance sensitive to

A

very sensitive to change in diameter of vessel

517
Q

what three factors effect flow

A

viscosity
diameter
length

518
Q

what is vascular distensibility

A

the fractional increase in volume for each mmHg rise in pressure

519
Q

what is vascular capacitance

A

the total quantity of blood that can be stored in a given portion of the circulation for each mmHG

think capacitance more like compliance

520
Q

what happens when veins are constricted

A

large quantities of blood are transferred to the heart and increases the cardiac output

521
Q

what factors contribute to mean pressure

A

cardiac output
peripheral resistance

522
Q

what factors contribute to pulse pressure

A

Stroke volume—increases in
stroke volume increases pulse pressure, conversely decreases in stroke volume decreases pulse pressure.

Arterial compliance—decreases in compliance
increases pulse pressure, also increases in compliance decreases pulse pressure

523
Q

how does arteriosclerosis effect pulse

A

decrease in compliance of arterial tree

leads to increase in pulse

524
Q

Patent ductus arteriosus effects pulse contours

A

low diastolic pressure
high systolic pressure
very high pulse pressure

525
Q

aortic regurgitation effect pulse contour

A

condition associated with backward flow of blood through the aortic valve.

Low diastolic
high systolic pressure
leads to high pulse pressure

526
Q

how does aortic stenosis effect pulse contours

A

condition associated with diameter of aortic valve opening is reduced and flow of blood through the aortic valve is low.

Low systolic pressure leads to low pulse pressure

527
Q

why is the spleen important in circulation

A

serves as special reservoir for red blood cells

528
Q

what serves as reservoirs in the body circulation

A

spleen
liver
large abdominal veins
venous plexus

529
Q

what is central venous pressure

A

pressure in the right atrium

usually 0-8mmHg

530
Q

how is right arterial pressure regulated

A

balance between
-the ability of the heart to pump
blood out of the atrium

-the rate of blood flowing into the
atrium from peripheral vein

531
Q

what factors increase right atrium pressure

A

– increased blood volume
– increased venous tone
– dilation of arterioles
– decreased cardiac function

532
Q

what happens when pressure is increased in right atrium

A

cause blood to back up into the venous system

abd pressure and venous pressure in legs increase

533
Q

what is in the veins to help keep low venous pressure

A

valves and muscle pump to maintain low venous pressure

534
Q

what can faulty venous valves lead to

A

varicose veins

535
Q

how do tissues control its own blood flow

A

it controls it in proportion to its own needs

536
Q

tissue needs include

A
  1. delivery of O2 to tissue
  2. nutrients ( glucose, amino acids, etc)
  3. remove CO2 and other metabolites
  4. transport hormones and other substances to different tissues
537
Q

what is flow closely related to

A

metabolic rate of tissues

538
Q

increases in tissue metabolism leads to

A

increase in blood flow

539
Q

decreases in O2 availability to tissues

A

increases blood flow

540
Q

what are the determinants of blood flow

A

pressure difference
resistance

541
Q

what are vasodilator substances

A

adenosine
CO2
lactic acid
ADP compounds
histamine
K ions
H ions
nitric oxide

542
Q

increase in tissue O2 concentration=

A

decrease in blood flow

543
Q

how do changes in tissue O2 concentration effect blood flow?

A
544
Q

define autoregulation

A

ability of a tissue to maintain blood flow relatively constant over a wide range of arterial pressures

545
Q

define metabolic theory

A

suggests that as arterial pressure is decreased, O2 or nutrient delivery is decreased resulting in release

546
Q

myogenic theory

A

proposes that as arterial pressure falls the arterioles have an intrinsic property to dilate in response to decreases in wall tension

547
Q

Law of Laplace

A
548
Q

long term local blood flow regulation occurs by

A

changing the degree of vascularity of tissues (size and number of vessels)

549
Q

what is an important stimulus for regulating tissue vascularity

A

Oxygen

550
Q

what factors does angiogenesis occur in repsonse to

A
  1. ischemic tissue
  2. rapidly growing tissue
  3. tissue with high metabolic rates
551
Q

what small peptides are angiogenic factors

A

-Vascular endothelial cell growth factors (VEGF)
-fibroblast growth factor (FGF)
-angiogen

552
Q

Vasoconstrictors

A

norepinephrine
epinephrine
angiotensin II
vasopressin
endothelin

553
Q

vasodilators

A

bradykinin
serotonin
histamine
prostaglandins
nitric oxide

554
Q

what role does the nervous system have in regulation of the circulation

A

-redistribution of blood flow
-increasing pumping activity of the heart
-rapid control of arterial pressure
-regulates via the ANS

555
Q

what is sympathetic nervous system in important control of

A

circulation

556
Q

what does PNS regulate

A

heart function

557
Q

what do sympathetic nerve fibers innervate all vessels except

A

capillaries
precapillary sphincters
some metarterioles

558
Q

what does innervation of small arteries and arterioles allows

A

sympathetic nerves to increase vascular resistance

559
Q

what are also sympathetically innervated

A

large veins
heart

560
Q

what is the PNS mainly in control of

A

heart rate via vagal nerve

561
Q

where is sympathetic vasoconstrictor system less potent

A

coronary circulation and the brain

562
Q

arterial pressure=

A

cardiac output x SVR

563
Q

arterial pressure can be increased by

A

-constricting almost all arterioles of the body which increases SVR

-constricting large vessels of the circulation thereby increasing venous return and cardiac output

-directly increasing cardiac output by increasing heart rate and contractility

564
Q

where is the VMC located

A

bilaterally in the reticular substance of the medulla and the lower 1/3 of the pons

565
Q

what is the VMC is composed of

A
  • vasoconstrictor area
    -vasodilator area
    -sensory area

located behind the pons in the medulla

566
Q

what are some functions VMC

A

-transmits signals continuously to sympathetic nerve fibers called sympathetic vasoconstrictor tone

-lateral portion controls heart activity by increasing heart rate and contractility

-medial portion transmits signals via vagus nerve to heart to decrease heart

567
Q

what is the neurotransmitter for the vasoconstrictor nerves

A

norepineprhine

568
Q

what else can have powerful excitatory and inhibitory on VMC

A

hypothalamus
amygdala

569
Q

the nervous system via the VMC can increase arterial pressure within seconds by

A

-constricting almost all arterioles of the body which increases total SVR

-constricting large vessels of the circulation thereby increasing venous return and cardiac output

-directly increasing cardiac output by increasing heart rate and contractility

570
Q

how are signals from the carotid sinus transmitted

A

herings nerve to glossopharyngeal nerve to nucleus tractus solitarius of the medulla

571
Q

how are signals from arch of aorta

A

through vagus nerve to nucleus tractus solitarius

572
Q

what are chemoreceptors sensitive to

A

lack of O2
excess CO2
H ion excess

573
Q

where are carotid bodies located

A

near carotid bifurcation
aortic arch

574
Q

when are chemoreceptors stimulated

A

when pressure falls below 80 mmhg

575
Q

what is one of the most powerful activators of the sympathetic vasoconstrictor system

A

CNS ischemic response

576
Q

when does CNS ischemic response get activated

A

below 60mmhg

greatest activation at 15-20 mmHg

577
Q

activation of low pressure receptors enhances

A

-Na and water excretion by decreasing rate of ADH
-increasing GFR
-decreasing Na reabsorption

578
Q

why is the bainbridge reflex important

A

prevents damming of blood in veins, atria and pulmonary circulation

579
Q

describe the bainbridge reflex

A

increase in atrial pressure increases the heart rate

stretch of atria sends signals to VMC via vagal

580
Q

the increase in arterial pressure causes the kidneys to

A

lose Na and water which returns extracellular fluid volume to normal (ECFV)

581
Q

what is pressure diuresis

A

the effect of pressure to increase water excretion

582
Q

what is pressure natriuresis

A

the effect of pressure to increase Na excretion

583
Q

what are the major determinants of long term arterial pressure control

A

-renal function curve
-salt and water intake line

584
Q

what leads to long term changes in arterial pressure

A

changing renal vascular resistance

585
Q

how does Na determine extracellular fluid volume (ECFV)

A

-As Na intake is increased, Na stimulates drinking, increased Na concentration stimulates thirst and ADH secretion.

-Changes in Na intake lead to changes in extracellular fluid volume (ECFV).

-ECFV is determined by the balance of Na intake and output.

586
Q

how is angiotension I turned to angiotensin II

A

AI is converted to AII by a converting enzyme located in the endothelial cells in the pulmonary circulation

587
Q

how is angiotensin I made

A

Renin acts on angiotensinogen to form angiotensin I

588
Q

where is renin

A

Renin is synthesized and stored in modified smooth muscle cells in afferent arterioles of the kidney.

589
Q

how does renin effect the angiotension system

A

-Causes vasoconstriction

-Causes Na retention by direct and indirect acts on the kidney

-Causes shift in renal function curve to right

590
Q

what factors decrease renal excretion and increase blood pressure

A

-angiotensin II
-aldosterone
-sympathetic nervous activity
-endothelin

591
Q

what factors increase renal excretion and reduce blood pressure

A

-atrial natriuretic peptide
-nitric oxide
-dopamine

592
Q

secondary causes of HTN

A

Renal artery stenosis
Chronic renal disease
Primary hyperaldosteronism
Sleep apnea
Pheochromocytoma
Preeclampsia
Aortic coarctation

593
Q

how does renal artery stenosis effect BP

A

Renal artery disease can cause of narrowing of the vessel lumen (stenosis).

The reduced lumen diameter in renal artery increases reduces the pressure at the afferent arteriole in the kidney.

Reduced renal perfusion stimulate renin release by the kidney. This increases circulating angiotensin II (ANGII) and aldosterone.

These hormones increase blood volume by enhancing renal reabsorption of sodium and water. Increased ANGII also causes systemic vasoconstriction.

The net effect of these renal mechanisms is an increase in systemic vascular resistance and an increase in cardiac output (transient).

594
Q

how does chronic renal disease effect BP

A

When this occurs, the kidney cannot excrete normal amounts of sodium which leads to sodium and water retention, increased blood volume. Renal disease may also result in increased release of renin leading to a renin-dependent form of hypertension.

The elevation in arterial pressure secondary to renal disease can be viewed as an attempt by the kidney to increase renal perfusion and restore glomerular filtration.

595
Q

what are some lifestyle changes to treat HTN

A

Losing weight if you are overweight or obese.

Quit Smoking

Eating a healthy diet,

Reducing the amount of sodium in your diet to 2,300 milligrams
Getting regular aerobic exercise

Limiting alcohol to two drinks a day for men, one drink a day for women

In addition to lowering blood pressure, these measures enhance the effectiveness of antihypertensive medications.

596
Q

medical treatment for HTN

A

There are several types of drugs used to treat hypertension, including: -Agnomens converting enzyme (ACE) inhibitors
-Angiotensin receptor blockers (ARBs)
-Diuretics
-Beta-blockers
-Calcium channel blockers

Diuretics are usually recommended as the first line of therapy for most people who have hypertension.

597
Q

what are 4 factors that can directly affect CO

A

the basic level of body metabolism

whether the person is exercising

the person’s age, and

the size of the body

598
Q

what is cardiac index

A

cardiac index (CI), which is the cardiac output per square meter of body surface area

599
Q

frank starling law of the heart

A

Increased quantities of blood flow into the heart stretches the walls of the heart chambers that causes cardiac muscle to contract with increased force

600
Q

what has direct effect on rhythmicity of heart

A

Stretch of the sinus node in the wall of the right atrium has a direct effect on the rhythmicity of the node to increase the heart rate as much as 10–15%.

601
Q

factors that cause a hypereffective heart

A

Sympathetic stimulation and parasympathetic inhibition does two things to increase the pumping effectiveness of the heart:
-It greatly increases the heart rate
-It increases the strength of heart contraction .

602
Q

Some of the factors that can decrease the heart’s ability to pump blood are the following:

A

Increased arterial pressure against which the heart must pump, such as in severe hypertension

Inhibition of nervous excitation of the heart

Pathological factors that cause abnormal heart rhythm or rate of heartbeat

Coronary artery blockage, causing a “heart attack”

Valvular heart disease

Congenital heart disease

Myocarditis, an inflammation of the heart muscle

Cardiac hypoxia

603
Q

Decreased cardiac output caused by cardiac factors

A

Severe coronary blood vessel blockage and consequent myocardial infarction

Severe valvular heart disease

Myocarditis

Cardiac tamponade

Cardiac metabolic derangements

604
Q

factors that affect venous return

A

Right atrial pressure,

Degree of filling of the systemic circulation

Resistance to blood flow between the peripheral vessels and the right atrium (resistance to venous return)

605
Q

What’s average map in aorta

A

94-96 mmHg

606
Q

What’s the average map in capillaries

A

16mmHg

607
Q

What is the most important endothelial derived relaxing factor

A

Nitric oxide

A lipophilic gas that is released from endothelial cells in response to a variety of chemical and physical stimuli

608
Q

What vasoconstrictor stimulates NO

A

Angiotensin II

609
Q

What is the big importance of angiotensin II

A

Acts on many arterioles of the body at the same time to increase SVR

Decreases sodium and water excretion by the kidneys to increase arterial pressure

610
Q

What is a major function of vasopressin

A

Greatly increases water transportation from the renal tubules back into the blood to help control body fluid volume

611
Q

What does increase in Ca ions cause

A

Vasoconstriction

612
Q

What does increase in k ions cause

A

Vasodilation

613
Q

What does increase in Mg ions cause

A

Powerful vasodilation

614
Q

What does increase in H ions cause

A

Large decreases in pH cause Dilation in arterioles

*slight decrease in H ions concentration can cause arteriolar constriction

615
Q

How do anions effect blood vessels

A

Acetate and citrate can cause mild vasodilation

616
Q

What can increased CO2 cause in blood vessels

A

Moderate vasodilation in tissues

marked vasodilation in the brain

617
Q

What 2 ways can angiotensin II act on the kidneys

A

1 acts directly on the kidneys to cause Na and water retention

2 causes adrenal glands to secrete aldosterone to increase salt and water absorption in kidney tubules

618
Q

Characteristics of primary HTN caused by excess weight gain and obesity

A

-cardiac output increased
-sympathetic nerve activity (especially in the kidneys) is increased in overweight patients
-angiotensin II and aldosterone levels are increased twofold to threefold in obese patients
-renal pressure natriuresis mechanism is impaired

619
Q

What 3 mechanisms show blood pressure responses in seconds

A

Baroreceptor feedback
CNS ischemia
Chemoreceptor mechanism

620
Q

What blood pressure mechanisms react after minutes

A

-rasa vasoconstrictor mechanism
-stress/relaxation of vasculature
-shift of fluid through tissue capillary walls

621
Q

Cardiac output =

A

Arterial pressure / svr (total peripheral resistance)

622
Q

Two types of factors that can make the heart a better pump than normal:

A

Nervous stimulation

Hypertrophy of the heart muscle

623
Q

What three principles factors affect venous return to the heart

A
  1. Right atrial pressure
  2. Degree of filling of systemic circulation (mean systemic filling pressure)
  3. Resistance to blood flow between the peripheral vessels and right atrium
624
Q

how long does it take to transmit a signal from SA node to AV node

A

0.03 sec

625
Q

what is the time from AV bundle to last of ventricular fibers

A

0.06 sec

626
Q

how much faster is systole than diastole

A

1/3 faster

627
Q

where does repolarization start

A

apex of the heart

last to depolarize is first to repolarize

628
Q

how much does HR increase with 1 degree increase in body temp

A

10 bpm

629
Q

long QT syndrome can be caused by which electrolyte imbalances

A

hypomagnesemia
hypokalemia

can lead to torsades

A & P I (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions