Physiology Flashcards
(185 cards)
1
Q
Three pressures in the CV system?
A
- Driving (difference between two points)
- Hydrostatic (P of gravity and weight of blood)
- Transmural (P of blood on vessel wall)
2
Q
Arteriolar resistance is regulated by the _1_ nervous system.
A
- Autonomic
3
Q
Arteries are under _1_ pressure and Veins are under _2_ pressure.
A
- High
- Low
4
Q
Blood flows from __1 (high/low)__ pressure to __2 (high/low)__ pressure. The __3__ drives blood flow.
A
- High
- Low
- Pressure gradient
5
Q
Blood flow is inversely proportional to the _1_ of blood vessels. When blood flow increases, _1_ has decreased.
A
- Resistance (nothing is holding it back)
6
Q
What is the equation for blood flow/cardiac output/Q?
A
CO = (Mean arterial pressure [highest P] - Right arterial pressure [lowest P]) / (Total peripheral resistance [TPR])
7
Q
What are the factors that change the resistance of blood vessels (3)?
A
- Viscosity of blood (numerator)
- Length of blood vessel (numerator)
- Radius of blood vessel to the fourth power (denominator)
Resistance = (8*visc*length)/(pi*r^4)
8
Q
What is viscosity?
A
Increased viscosity is due to increased internal friction.
- thickness
- the state of being thick, sticky, and semifluid in consistency
- a measure of its resistance to gradual deformation by shear stress or tensile stress
9
Q
Increasing viscosity by increasing hematocrit will _1_ resistance and _2_ blood flow.
A
- increase
- decrease
10
Q
Increasing the length of a vessel will _1_ resistance. Increasing the radius of a vessel _2_ resistance.
A
- increase
- decrease
11
Q
If a blood vessel radius decreases by a factor of 2 then resistance _1_ by a factor of _2_ and blood flow _3_ by a factor of _4_.
A
- increases
- 16
- decreases
- 16
12
Q
_1_ resistance is illustrated by systemic circulation. Each artery in _1_ receives a fraction of the total blood flow.
A
Parallel
13
Q
When an artery is added in parallel, the total resistance _1_. In each parallel artery, the pressure is the _2_.
A
- decreases
- same
14
Q
_1_ resistance is illustrated by the arrangement of blood vessels in a given organ. _2_ are the largest contributers to this resistance.
A
- Series
- Arterioles
15
Q
As blood flows through the series of blood vessels, pressure _1_. Each blood vessel in series receives the _2_ total blood flow.
A
- decreases
- same
16
Q
_1_ flow is streamlined. _2_ flow is not and causes audible vibrations called _3_.
A
- Laminar
- Turbulent
- bruits
17
Q
A _1_ number predicts whether blood flow will be turbulent or laminar.
A
Reynold’s number
18
Q
An increased Reynold’s number increases the likelihood of _1 (laminar/turbulent)_ flow.
A
turbulent
19
Q
What are the two factors that increase a Reynold’s number?
A
- Decreased blood viscosity (ex. anemia, lower hematocrit)
- Increased blood velocity (ex. narrowing of a vessel [decreased radius)
20
Q
What is hematocrit?
A
the volume percentage of red blood cells in blood
21
Q
Pulse pressure is the difference between _1_ and _2_ presures.
A
- systolic
- diastolic
22
Q
Aging leads to a _1_ in capacitacne and an _2_ in pulse pressure.
A
- decrease
- increase
23
Q
When is systolic pressure measured?
A
**After **the heart contracts (systole) and blood is ejected in the **arterial **system.
24
Q
When in diastolic pressure measured?
A
When the heart is relaxed (diastole) and blood is returned to the heart via the veins.
25
Systolic pressure is the \_1 (highest/lowest)\_ **arterial** pressure during a cardiac cycle. Diastolic pressure is the \_2 (highest/lowest)\_ **arterial** pressure during a cardiac cycle.
1. highest
2. lowest
26
Mean arterial pressure = ?
MAP = 1/3 Systolic P + 2/3 Diastolic P
\*because most of the cardiac cycle is spent in diastole
27
Venous pressure is very \_1 (high/low)\_. Veins have a \_2 (high/low)\_ capacitance and therefore can hold \_3 (large/small)\_ volumes of blood at low pressure.
1. low
2. high
3. large
\*Capacitance is proportional to volume (numerator) and inversely proportional to pressure. As a person ages, their arteries become stiffer and less distensible/stretchy therefore capacitane of arteries decreases with age.
28
what are 4 methods of regulating arterial blood pressure?
1. Increase pumping force
2. contract veins and arterioles
3. infuse fluids
4. administer vasoconstrictors
29
which ventricle has a thicker muscular layer? why?
the left ventricle. It must pump blood through to aorta to systemic circulation.
30
how does the heart contract?
in a spiral contraction (like wringing a washcloth)
31
what is the % ejection volume referring to?
the amount of blood pushed out of the ventricles
32
capillaries have (high/low) velocity, (high/low) resistance and (high/low) cross-sectional area.
low
low
high
33
arterioles have the (highest/lowest) resistance
highest
34
Describe the normal sequence of cardiac depolarization: conduction of AP atrium --\> ventricle
SA node--\>(artium)--\>AV node--\>bundle of His--\> L/R bundle branches --\> purkinje fibers --\> (ventricle)
35
Describe the normal sequence of VENTRICLE repolarization
epicardium --\>endocardium
base--\>apex
\*\*AP shorter in epicardium
36
Define the standard bipolar limb leads and Einthoven's triangle
3 bipolar limb leads:
lead1: RA--\>LA
lead2: RA--\>LL
lead3: LA--\>LL
(-) --\> (+)
einthoven's triange
37
Define the augmented unipolar limb leads and Wilson's central terminus
3 unipolar limb leads:
aVR: right arm
aVl: left arm
aVf: left leg
38
basic definition of EKG
mean cardiac vector is assessed in several leads
records cardiac electrical activity over time
examines how action potential is generated/conducted through heart
non-invasive electrodes on skin
39
ECG: Identify the P, Q, R, S, and T waves
P- atrial depolaization
A-V delay
QRS- ventricular depolarization
plateau
T- ventricular repolarization
40
Identify the PR interval, QT (QTc) interval, ST segment.
these segments might change if A-V conduction is delayed, the ventricular action potential is prolonged, or the heart becomes ischemic.
41
Given an ECG record, determine the mean QRS axis and classify it as normal, left-, or right-deviated.
Left axis deviation: -30 to -90
Normal mean QRS axis -30 to +90
Right axis deviation +90 to +180
42
functional syncytium: how does cardiac eletrical activity travel through heart
action potential is conducted cell-to cell by direct coupling
cells connected by intercalated disks and gap junctions
43
how does a cardiac electical signal make a heart beat
action potential --\> intracellular calcium transport --\> contraction force
44
what is the "pacemaker potential" or "automaticity" in cardiac myocytes
specialized cells that can cause their own AP/depolarization
nodes= impulse generation sites
control heart beat
\*SA node, AV node, purkinje fibers
45
how does parasympathetic neuronal input affect the heart?
parasympathetic--\>vagus nerve--\> acetylcholine --\> DECREASE heart rate
46
how does sympathetic neuronal input affect the heart?
sympathetic --\> T1-4 spinal nerves --\> norepinephrine --\> INCREASE heart rate
47
What is the spontaneous rate of the SA node?
70-80 AP's/min
\*\*main pacemaker
48
What is the spontaneous rate of the AV node?
40-60 AP's/min
49
What is the spontaneous rate of the purkinje fibers?
15-40 AP's/min
\*not a good pacemaker
50
what is the Frank-starling mechanism? how does it relate to the heart?
strength of contraction is proportional to the end diastolic volume/pressure
significance of atrial contraction: "kick" fills ventricle with blood
increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully
51
Why/HOW is conduction through the AV node very slow
allows for complete emptying of atrial blood into ventricle
slow Ca2+ channels take longer to develop AP and velocity reduced (versus fast Na+ channels in His/purkinje)
52
53
Describe the normal sequence of VENTRICLE depolarization: AP is conducted...
VENTRICLE depolarization: AP is conducted...
apex--\>base
endocardium --\>epicardium
54
total time from impulse initiation in SA node to repolarization of ventricles
~600 msec
55
Hexaxial Reference System
56
Describe the unipolar precordial/chest leads
all 6 (+)
V1-V6
records the AP in the horizontal plane
57
relationship of vectors to deflections of EKG: when do you have a (+) upstroke on EKG
when the mean cardiac vector is parallel and in SAME direction as EKG lead axis orientation
58
relationship of vectors to deflections of EKG: when do you have a (-) downward stroke on EKG
when the mean cardiac vector is parallel but OPPOSITE direction to EKG lead axis orientation
59
relationship of vectors to deflections of EKG: when do you have a biphasic signal on EKG
when the mean cardiac vector is PERPENDICULAR to the EKG lead axis orientation
60
Describe the QRS changes as the AP progresses through the unipolar precordial/chest leads
V1--\>V6
R wave increases
S wave decreases
\*zone of transition ~V3: R and S waves equal in amplitude
L ventricle has larger mass
61
how does the EKG change with decreased AV conduction ("conduction failure")
prolonged PR interval
62
how does the EKG change: ventricular pre-excitation ("wolfe-parkinson-white")
shortened PR interval
63
how does the EKG change: slow conduction through the ventricle or purkinje fibers (bundle branch block)
widened QRS duration
64
how does the EKG change: slow repolization of ventricles
long QT interval
\*increase risk for arrhythmias
65
what is a "corrected QTc interval"
as heart rate increases, the AP duration decreases, the QT interval decreases
66
how does the EKG change: ischemia
elevation or depression of ST segment (plateau of AP)
plateau of AP is not flat bc not all cells are depolarized
K+ channels open and AP shorten
67
how does the EKG change: subendrocardial ischemia
ST segment depression
68
how does the EKG change: epicardial ischemia
ST segment elevation
69
explain excitation-contraction coupling
electrical stimulation of the heart results in mechanical work
70
describe the sarcolemma around myocyte
specialized plasma membrane
contains T-tubules, SR's, and Ca2+ channels to trigger contractions
71
2 enzymes of the sarcoplasmic reticulum
calcium release channel (ryanodine receptor) and SR Ca2+-ATP-ase pump
to release and remove Ca2+ from cytoplasm during contraction
72
explain the calcium-induced-calcium release in myocytes
positive-feedback mechanism to amplify rise in cytoplasmic Ca
outside Ca influx triggers inside Ca release from SR
increases strength of contraction
73
describe crossbridge formation in myocytes
ATP hydrolyzed by myosin head
Ca binds to troponin C
conformation change of tropomyosin
reveals binding site on actin
crossbridge formation
power stroke
ADP released from myosin
new ATP binds myosin
myosin releases actin
74
the "treppe effect" or staircase phenom of cardiac muscle
effect of repetitive stimulation on force: increase [Ca] in SR= increase contraction force)
increased stimulation frequency= increase in Ca release= increased tension=
increase in contractile state
75
explain the law of La Place in cardiac performance
increased venous return= increase in diastolic filling= greater end diastolic volume= greater wall tension
76
cardiac performance: preload
ventricle wall tension prior to contraction
end diastolic volume stretches and determines the sarcomere length
increased preload= increased cardiac output
–pressure at end diastole used to estimate preload
77
explain Frank-Starling relationship in cardiac muscles
increased preload/end diastolic volume= increased cardiac performance
increase diastole = increase systole= increast cardiac output
78
cardiac performance: afterload
force aginst which the cardiac muscle is working in systole
limits ventricular performance
increased afterload= dec velocity= dec shortening of muscle fibers
–during systole, chamber radius falls, so afterload decreases during ejection
79
4 major variables of effective cardiac output
1 contractile state
2 preload
3 afterload
4 heart rate
80
effects of a (-) inotroph on myocardium contractility
decrease contractility
ex) Acidosis, ischemia, Ca channel blocking drugs, and Β-adrenergic blockers
81
effects of a (+) inotroph on myocardium contractility
increase contractility
ex) NE, catechols, Digoxin, Drugs that Increase Ca availability to sarcomeres;
increase preload; increase CO
82
how does the B-adrenergic receptor system affect the heart
autonomic nervous system increases nodal depolarization and strength of contraction
B-adrenergic stimulation: inc Ca= increase contraction
inc uptake by SR= faster relaxation
\*\*most important single mediator of cardiac perfomance due to effects on contractility, relaxation, and rate
83
Cardiac vs. Skeletal Muscle: how to vary force of contraction
* Both types can vary force of contraction by changing fiber length
* Only skeletal muscle can increase force through increasing frequency of stimulation
* Only cardiac muscle can increase force through increasing contractility
84
what is the Z-band
Z Band: End of sarcomere, Site of interclated disk, Site of insertion for thin filaments, Site of “triad”: (the T tubule, Ca channel, and SR meet)
85
define contractility in myocardium
•Cardiac muscle increases strength of contraction through changing contractility
•the contractile state determines:
–The velocity of muscle fiber shortening
–Extent of shortening
•Determined by [Ca2+]i
•
86
myocardium: Increasing preload
Increasing preload increases
the velocity and extent of shortening if afterload is constant
87
myocardium: Increasing afterload
Increasing afterload reduces
the velocity and extent of
shortening for any given preload
88
Cardiac vs Skeletal muscle: contraction
•Cardiac muscle contraction requires extracellular Ca2+
–CICR triggered by influx of calcium from outside cell
–skeletal muscle contraction triggered by AP directly; CICR does not require Ca influx
•Skeletal muscle can increase force by recruitment of other cells
•Cardiac muscle is a functional synctitium, all cells contract and relax together
89
myocardium: what changes in the sarcome during contraction
* The length of the filaments does not change
* Z line to Z line distance gets shorter
* H band and I band get shorter
* A band does not change in size
90
how are the semilunar and atriventricular valves opened?
high pressure in the ventricles and atria, respectively
91
what is the difference in ventricular activity for diastole and systole?
diastole is ventricular filling (relaxation), systole is ventricular emptying (contraction)
92
what is happening during the P wave?
atrial depolarization
93
What is happening during the T wave?
ventricular **repolarization** until ventricular **relaxation**
94
what is happening during the QRS complex?
ventricular **depolarizaton** to ventricular **contraction**
95
what are the 5 stages of the left ventricular pressure-volume loop?
1. isovolumetric contraction
2. ejection (period between aortic valve opening and closing)
3. isovolumetric relaxation
4. rapid ventricular filling (as soon as mitral valve opens)
5. slow ventricular filling (right before MV closes)
96
what is happening in isovolumetric contraction?
beginning of ventricular systole (contraction) but the aortic valve is closed therefore volume does not change but pressure is rising quickly.
\*valves are closed because pressure in aorta is higher than pressure in the ventricle
97
the period of rapid ejection begins when pressure within the ventricle is \_1\_ compared to the aorta or pulmonary artery?
1. greater
98
In isovolumetric relaxation, there is a \_1\_ in ventricular pressure.
It ends when there is what kind of relationship between the ventricle and atrium?
1. decrease
when the pressure in the ventricle falls below the atrium
99
What does the *a* wave represent in the atrium?
atrial contraction.
\*follows P wave of EKG
100
what does the c wave represent?
ventricular contraction
101
what does the x descent represent (3)?
1. ventricular emptying
2. thoracic volume and pressure fall
3. rapid fall in atrial pressure
102
what does the v wave represent?
flow of blood from veins to atria.
\*long period of time, AV valves are closed
103
the v wave corresponds roughly with which segment of the EKG?
ST segment
104
the *y *descent represents what?
* atria draining into the ventricles
* rapid fall in atrial pressure
105
What does the S1 heart sound represent?
"LUB"
the mitral and tricuspid valves closing (AV valves)
\*at this time the AoV and P valve are opening quietly
end diastole
slow, low pitched sound
106
What are you hearing with the S2 heart sound?
"DUB"
aortic and pulmonary valve closure
\*as MV and TV valves open quietly
end of systole
rapid, high frequency sound
107
What are you hearing with the S3 heart sound?
mitral regurgitation (preload is high, pressure in ventricle increases and MV opens as a result of increased pressure)
108
what are you hearing with the S4 heart sound?
atrial contraction: the left atrium pushing against a stiff left ventricle
* high atrial pressure
* may lead to ventricular hypertrophy
109
S4 occurs during with segment of the EKG? Which part of the jugular pulse curve?
P-Q interval; a wave (aortic contraction)
110
S1 occurs during which part of the EKG diagram? jugular pulse?
* QRS complex (mainly RS when isovolumentric contraction ends)
* c wave (ventricular contraction)
111
S2 occurs during what part of the EKG?
at the end of the T wave when the ventricle has finished emptying
112
What are the 3 types of cardiac action potentials?
- ventricular- atrial- nodal
113
Describe each of the phases (5) of cardiac action potentials.
0: rapid depolarization 1: brief, partial repolarization (absent in nodal)2: plateau (shorter in atrial, absent in nodal)3: complete repolarization (back to resting or pacemaker)4: resting potential (ventricular & atrial) or pacemaker potential (nodal)
114
Nodal action potentials differ from atrial and ventricular in that they lack which phases?
Nodal APs lack phases 1 and 2
115
Which type of cardiac APs are significantly slower (takes longer from start to finish) than the others?
Nodal is much slower than atrial or ventricular
116
Which ion is responsible for depolarization in each of the cardiac AP types?
Ventricular and Atrial: Na+ influxNodal: Ca^2+ influx
117
Describe the difference between resting potential (phase 4) in the 3 types of cardiac APs.
Atrial and ventricular (resting potential) is constant at about -80 mVNodal (pacemaker potential) slowly depolarizes toward threshold (max hyperpolarization is -60 mV) due to the "funny" Na+ that open on hyperpolarization
118
Why is pacemaker potential not constant?
Pacemaker potential in nodal APs slowly depolarizes because the "funny" Na+ channels are open during hyperpolarization
119
How to cardiac APs control heart rate?
the frequency of nodal APs control heart rate (the duration of phase 4 will lengthen or shorten)
120
In general, what ion conductances does the autonomic nervous system alter to change heart rate? (3)
1. Na+2. K+3. Ca^2+
121
How does the parasympathetic nervous system slow the heart rate?
Vagus nerve: releases ACh- depolarize the threshold - decreases Na+ and Ca^2+ permeability and increases K+ permeability during pacemaker potential (hyperpolarization)
122
How does the sympathetic nervous system increase heart rate?
Release of norepinephrine during pacemaker potential- increases Na+ and Ca^2+ potential and decreases K+ permeability (depolarizes)
123
normal EKG values: PR interval
PR interval=
120-200ms,
.12-.20s
124
normal EKG values: P wave
P wave:
60-100ms,
.06-.10s
125
normal EKG values: QRS duration
QRS duration
60-100ms,
.06-.10s
126
Normal EKG values: QT interval
QT interval
450ms, .
45ms
127
myocardium: ischemia vs infarction
ishemia- restriction in blood supply/can be reversed
infarction- necrosis/damage/not reversible
128
stable vs unstable angina
no ekg changes, can have changes in lab values for cardiac enzymes
stable: predictable pain, on exertion, goes away with rest
unstable: changes from usual pattern, at rest
129
normal heart rates by age
Infants: 100 to 160 beats per minute
Children 1 to 10 years: 70 to 120 beats per minute
Children over 10 and adults: 60 to 100 beats per minute
Athletes: 40 to 60 beats per minute
130
types of aortic stenosis (3)
vallvular
131
signs of severe aortic stenosis (3)
1. delayed, small volume carotid upstroke (turbulance= shuddering of valve)
2. loss of A2
3. late peaking murmur
on top of common aortic stnosis sx: CP, DIB, syncope, heart failure signs, JVD, S4
132
in the clinic: why do we make patients stand or valsalva
reduce venous return
reducec systolic
decrease aortic pressure
increase heart rate
shrink heart
make murmurs worse (HCM and MVP)
133
hypertrophic cardiomyopathy
buldging of septum into outflow tract
occurs as midsystolic murmur
heard best at LLSB
brisk carotid upstrokes, no ejection sound
murmur increases with standing/valsalva
most common in young people with sudden loss of consciousness
134
describe pulmonic stenosis and associated heart sound
obstruction of flow from the right ventricle of the heart to the pulmonary artery
inc resistance to blood flow causes right ventricular hypertrophy
midsystolic ejection murmur that does NOT radiate to carotids
widened S2 split
varies with respiration
135
describe an innocent systolic murmur
caused by high flow in outflow tracts
"stills murmur" in children
crescendo-decrescendo ejection murmur
common in pregnancy, anemia, fever, high output state
localized to pulmonic or aortic area
136
describe a holosystolic or "pansystolic" murmur
(2 types)
begins with SA and end after S2
caused by high flow
harsh, blowing, well heard with diaphragm
1. AV valve leakage
2. interventricular shunt
137
chronic mitral regurgitation and associated heart sound
caused by mitral valve prolase
leads to chronic volume overload of L ventricle
can hear at axilla and base
increases with inceased afterload (squatting)
holosystolic murmur (from S1 through S2; pansystolic)
S3
harsh/ blowing sound
138
describe mitral valve prolapse and associated heart sound
mitral leaflet moves into LA suring systole
causes mild systolic "click"
can cause regurgitation
139
describe mitral stenosis and associated heart sound
narrowing of the heart's mitral valve= decreased blood to L ventricle
turbulent, high velocity flow in diastole
mainly caused by rheumatic heart disease
can cause atrial fibrillation
rumbling diastolic murmur: opening snap, loud S1
OS= sharp
140
signs of severe mitral stenosis
long diastolic rumble (pandiastolic)
short A2-OS interval
pulmonary hypertension= loud P2 and RV lift
artial fibrillation
CHF
141
aortic regurgitation and associated heart sound
incompetant aortic valve
loss of cardiac output backwards from aorta into LV
LLSB with diaphragm (high frequency): S3
midsystolic murmur (MSM) and blowing, decrescendo early diastolic murmur (EDM)
best heard when pt leans forward and breathes out
bounding carotid pulse palpable (increased systolic arterial pressure)
142
PE findings: "water hammer pulses"
wide pulse pressure with low diastolic
Due to the large stroke volume and "aortic runoff" of blood from the aorta back into the left ventricle, there is a sudden rise and abrupt collapse of peripheral arterial pulse.
143
PE findings: Durrosiez's sign
to and fro bruit at femoral artery
144
PE findings: Hill's sign
popiteal arterial pressure \> 20 mmHg more than brachial
145
PE findings: Quinke's sign
Quincke's: pulsating capillary refill in slightly compressed fingernail bed
nailbed flush with systole
146
PE findings: de Musset's sign
deMusset's sign: bobbing of head with each heart beat
147
signs of severe aortic regurgitation
diastolic BP less than 50
enlarged LV (large regurgitant volume)
S3
CHF sx
bounding (Corrigan's) pulses
148
in the clinic: why do we make patients squat during cardiac exam
increase venous return
increase venous return
increase murmurs (AS and MR)
149
physiological splitting of S2
normal sound
asynchronous A2 aortic and P2 pulmonic valve closure
heard on inspiration over pulmonic valve
inspiration draws more blood into expandedlungs and RA/RV
increased duration of left ventricular systole
\*these change with respiration
150
abnormalities of S2
```
loud P2/ audible at apex= hypertension
single S2 (A2 OR P2 MISSING)
WIDE S2 SPLITTING
PARADOXIAL SPLITTING (P2 before A2)
\*these not change with respiration
```
151
abnormalities of S2: what can cause a wide S2 splitting
pulmonic stenosis, mitral regurgitation, R bundle branch block, atrial septal defect
152
abnormalities of S2: what can cause a loud S2 heard even at the apex
loud P2/ audible at apex= hypertension
153
what disease does hearing an S3 indicate?
volume overload
rapid filling of diastole
154
what disease does hearing an S4 indicate?
hypertension
hypertrophic cardiomyopathy
aortic stenosis
155
grading murmurs
1/6= less than S1/S2
2/6= murmur is equal S1/S2
3/6=murmur is greater than S1/S2
4/6= palpable thrill
5/6= heard with stethoscope
6/6= audible with naked ear
156
murmur patterns (4)
holosystolic
crescendo
decrescendo
crescendo-decrescendo
157
Corrigan's pulse
visibly bounding arterial pulse
common in carotid, brachial and femoral arteries with increased systolic arterial pressure
158
describe aortic stenosis and its related heart sound
aortic valve narrows
listen ay 2RICS: harsh crescendo-decrescendo midsystolic murmur (MSM)
S2 split
3LICS: sharp ejection sound (ES)
159
describe a holosystolic murmur
(HSM) fills the entire systole, and may even obscure the two heart sounds.
160
What dx alters the QRS on EKG
bundle branch blocks
abrnomal depolarization (VPC's)
myocardial disease
161
what is happening here?
increased venous return
162
what is happening here?
atrial contraction
increased venous return
increased pressure in right atrium
163
what is happening here?
no a wave
filling from right atrium to ventricle is high (sharp y curve)
x is small because atria doesn't relax
164
what is happening here?
increase PR interval. for the curve, nothing has changed from sinus rhythm because a first degree block is asymptomatic.
165
what is happening here?
high atrial contraction
166
what is happening here?
ventricle is not contracting
167
what is happening here?
atria are contracting but nothing else is working because the signal cannot get past the AV node.
168
two functions of the venous system?
blood storage/liberation, regulat return of blood to heart
169
#% of the total blood volume is contained in the venous system (think about earth)
70%
170
what is the effect of sympathetic stimulation on venous tone? how does that change blood flow?
venous tone increases, less blood is held in the veins.
171
CVP is also equal to what?
venous pressure equal right atrial pressure
172
Myocardial ischemia
insufficient blood flow
O2 delivery\< O2 demand
Leads to: heart failure (loss of systole/diastole), arrhythmia, tissue damage, dyspnea, angina pectoris
173
Collateral vessel
After a coronary artery occlusion, collateral vessels often develop to shunt blood around the blockage.
174
Physiologic role of conduit vessels in coronary circulation
Arteries and veins that supply the myocardium
175
Physiologic role of resistance vessels in coronary circulation
Precapillary arterioles that regulate flow to myocardium
176
Physiologic role of exchange vessels in coronary circulation
Capillaries that allow gas/nutrient exchange at myocardium
177
Physiologic role of capacitance vessels in coronary circulation
Venules that return blood from the myocardium to the heart
178
rate of Normal coronary blood flow
1ml/min/g myocardium at rest, and 4 ml/min/g with exercise
179
Acute vs subacute vs sustained state of myocardial ischemia
Acute is reversible (\<10min),
subacute is slowly reversible/"stunned" (10min-10hrs),
Sustained is irreversible/"infarcted"(\>10 hrs)
180
Name some mechanisms that control coronary blood flow
metaboliuc regulation- meet myocardium's demands
physical factos- pressure on vessel
physioligical response- changes due to NO or NE release
181
What happens if the MAP (mean arterial pressure drops below 50mmHg?
loss of blood flow to the coronary blood vessels and myocardium
vital organs will not get enough Oxygen perfusion, and will become hypoxic, a condition called ischemia.
182
what can happen if the diastolic intraventricular pressure is too high or if diastole is too short (ex due to rapid heart rate)
lack of blood flow to the coronary arteries and myocardium
myocardium perfusion occurs in DIASTOLE
183
What is MAP?
[MAP] is considered to be the perfusion pressure seen by organs in the body.
average arterial pressure during a single cardiac cycle
[MAP}= {2/3}(DP) + (1/3}(SP)]
[MAP = (CO \*SVR) + CVP]
184
describe this calculation for coronary afteries: Functional flow reserve (FFR)
Calculates pressure gradient in coronary artery before and after an obstruction/stenosis
FFR= P(distal)/P(aorta)
\*\*FFR\<.75 is BAD
185
describe this calculation: Coronary artery stenosis gradient
Measure perfusion pressure in coronary artery before and after an obstruction/stenosis
∆P= P(aorta)-P(distal)
