Cardiac Lecture 2 Flashcards
(97 cards)
1
Q
what is the equation for stroke volume
A
EDV-ESV
2
Q
what is the equation for EF
A
SV/ EDV
3
Q
equation for cardiac output
A
HR x SV
4
Q
what does pre-load refer to?
A
amount of blood returned to the heart/ the amount eh ventricles are stretched
5
Q
what does afterload refer to?
A
the amount of arterial pressure
6
Q
does cardiac output increase or decrease with age?
A
decrease
7
Q
what is the normal cardiac output for men?
A
5.6 L/min
8
Q
what is the normal cardiac output for a woman?
A
4.9 L/min
9
Q
what is the max cardiac output for an average person?
A
15-20 L/min (3X increase)
10
Q
does max HR increase or decrease in old age?
A
decrease
11
Q
equation for HR based on age
A
220-age = HR
12
Q
what is the gold standard to measure cardiac output
A
echocardiography
-measures SV by measuring blood flow through left ventricular outflow tract
13
Q
what is swan Ganz pulmonary wedge pressure
A
- measures cardiac output
- catheter in pulmonary artery and occludes vessel
- equal to left atrial pressure
14
Q
the Fick Principle
A
- measures cardiac output
- VCO2/ (Ca02-Cv02)
15
Q
the role of angiotensin II
A
- circulating hormone
- induce the release of Ca2+ in cardiac myocytes
- facilitates the release of NE from nerve terminals
- positive inotropic
16
Q
the role of thyroid hormones
A
- regulate metabolism
- positive chronotropic and inotropic effects
17
Q
the role of insulin
A
- increases the uptake of glucose
- positive inotropic effects
18
Q
the role of glucagon
A
- increases blood glucose
- chronotropic (increases cAMP) and inotropic effects
19
Q
what effect does hypokalemia have on the cardiac myocyte cells
A
low extracellular K+ increases the gradient so intracellular K+ will want to move out of the cell quicker
- inside of the cell becomes more negative as positive charge leaves
- HYPERPOLARIZATION of the cell membrane, makes harder to get an action potential
20
Q
what effect does hyperkalemia have on cardiac contraction
A
- high extracellular K+ decreases the gradient and causes DEPOLARIZATION
- muscle weakness from inadequate action potential
- blocks conduction
21
Q
what vessels serve as reservoirs for blood
A
- pulmonary circulation
2. veins, venues, and venous sinus
22
Q
what tissues does an artery have
A
- fibrous tissue
- elastic tissue
- both expand and contract rapidly - endothelium: to secrete nitric oxide
- smooth muscle: to constrict and vasodilate
23
Q
what tissues does the arteriole have
A
- endothelium
- smooth muscle
- major function is to constrict and dilate
- lot of smooth muscle and surface area to change blood flow to different tissues
24
Q
tissues of a capillary
A
- endothelium
- gas exchange; allows one RBC to pass at a time
25
tissues of a venule
1. endothelium
| 2. fibrous tissue
26
tissues of a vein
similar to arteries
27
what dictates flow and resistance of where the blood goes
arterioles
28
what is CO equation for flow
Change in pressure / resistance
| MABP- CVP/ SVR
29
systolic and diastolic pressure in the aorta
120/5
30
pressure in the systemic capillaries
17
31
central venous pressure
2= right atrium
32
systolic and diastolic pressure in the right ventricle
25/1
33
systolic and diastolic pressures in pulmonary arteries
25/8
34
pressure in pulmonary capillaries
7
35
pressure in pulmonary veins
2
36
what will happen to MABP if there is an increase in resistance but CO stays the same?
MABP will increase
37
what will happen to MABP if you increase CO with the same resistance?
MABP will increase
38
what two things effect pulse pressure
1. stroke volume
- the greater the SV the greater the PP
2. Compliance
- the less the compliance the greater the PP (systolic pressure)
39
equation for vascular compliance
change in volume/ change in pressure
40
does MABP increase or decrease with age?
increase
41
what is general term for hardening of the arteries
arteriosclerosis
42
4 side effects of arteriosclerosis
1. loss of compliance (hardening of arteries)
2. destroys endothelium ( reduces nitric oxide)
3. increase in systolic pressure (increase in afterload)
4. leads to hypertrophy and hypertension
43
the most common form of arteriosclerosis
atheroslerosis
| -plaque in arteries
44
the volume that passes a given point over time
flow rate ( how much)
45
distance the volume of blood will travel in time
velocity of flow (how fast)
46
equation for velocity
flow rate/ cross sectional area
| - the narrower the vessel the faster the velocity of flow
47
is velocity of flow proportional or inversely proportional to to cross sectional area
inversely proportional to cross sectional area
| -the bigger the cross sectional area, the slower the velocity of flow
48
what has the biggest cross sectional area
capillaries
| -good thing, allows more time for gas exchange
49
what has the slowest velocity of flow
capillaries
50
what has the fastest velocity of flow
aorta
51
3 things that determine resistance
1. length of the tube
2. viscosity of fluid
3. radius of the tube (biggest factor)
52
blood flow in series
R= R1 + R2 = R3
53
branching of blood vessels forms ____ circuit
parallel
R= 1/ (1/R1 + 1/R2 + 1/R3)
-less resistance, more flow
54
_____ are arranged in parallel
arterioles
55
the flow through individual arterioles is dependent on _____
resistance
56
increased resistance = _____ flow to that arteriole
decreased
57
blood is diverted from ___ resistance arterioles to ____ resistance arterioles
high, low
| -sympathetics can shunt blood away to other organs
58
arterioles control blood flow in ___ regions
local
59
total blood flow of all the arterioles in the body is always equal to
cardiac output
60
blood flow to individual tissues is possible because arterioles are arranged in
parallel
61
increase in metabolic products during tissue metabolism that induces vasodilation and increases blood flow
metabolic (active) hyperemia
| -autoregulation
62
will get ___ blood flow to an area of higher metabolism
more
63
5 vasodilators produces with increased tissue metabolism
1. CO2
2. K+
3. adenosine
4. H+ (acidosis)
5. phosphates
64
as arterial oxygen saturation decreases, blood flow will _____
increase
65
method of auto regulation of blood flow that causes endothelial cells to release NO and induce vasodilation
shear stress
66
vasoconstriction; released by endothelium
endothelin
67
vasoconstriction; secreted by posterior pituitary
vasopressin (antidiuretic hormone)
68
mostly vasoconstriction; released by platelets; intestine
seretonin
69
vasoconstriction; released by platelets; smooth muscle
thromboxane
70
vasodilation; released by endothelial cells
prostacyclin; PGI2
71
vasodilation; in blood plasma; released during inflammation
bradykinin
72
vasodilation; released during inflammation; allergies by mast cells
histamine
73
vasodilation; released by heart during stretch
ANP and BNP
74
what is the biggest dictator of blood flow in the heart
metabolism ( metabolic hyperemia)
75
3 things that alter coronary blood flow
1. contraction
2. metabolism
3. neuronal control (alpha and beta receptors)
76
the carotid sinus has baroreceptors associated with _____nerve
glossopharyngeal
77
the aortic arch has baroreceptors associate with the ____ nerve
vagus
78
where do the baroreceptors travel to signal what the blood pressure is
medulla
79
when the blood pressure increases, the baroreceptors fire ____ action potentials
more
80
these constantly send action potentials to the brain and alert the medulla what the blood pressure (MABP) is
baroreceptors
81
what happens when you have a high BP sensed by the baroreceptors
- sensed by baroreceptors in the carotid sinus and aortic arch
- this increases firing in the glossopharyngeal nerve and vagus nerve
- action potentials reach medulla
- medulla sends a vagal efferent output to SA and AV node to decrease HR and decrease CO and decrease BP
- inhibit sympathetics
82
what happens when you have a low BP
same as high blood pressure but slow action potentials and medulla sends vagal efferent to SA and AV node to increase HR, increase CO, and increase BP
-inhibit parasympathetics
83
condition when baroreceptors do not work properly
orthostatic hypotension
84
2 long term regulations of BP
1. antidiuretic hormone
| 2. RAAS system
85
where is the antidiuretic hormone (vasopressin) released from?
posterior pituitary when you have low BP or low blood volume
86
mechanism of antidiuretic hormone
1. promotes water retention
- kidneys excrete water and blood vessels reabsorb the water
2. vasoconstriction
87
mechanism of the RAAS system to raise BP
1. low BP is sensed by kidneys
2. increase renin production
3. renin convertis angiotension (liver) to angiotension I
4. in the prescence of ACE from the lung/ kidneys, angiotension I is converted to angiotension II
5. angiotension II activates the sympathetic nervous system and cause Na+ reabsorption and water retention
6. adrenal cortex secretes aldosterone that also helps with Na+ retention and water retention
7. angiotension II induces vasoconstriction
8. induces secretion of ADH from posterior pituitary to promote water reabsorption
88
the best target for hypertension
RAAS system
89
why does obesity correlate with hypertension
adipocytes carry angiotension, renin, angiotension I, and ACE--- all necessary for aldosterone and Angiotension II to promote vasoconstriction and increase Na+ and water reabsorption
90
atrial and brain natriuretic peptides
another mechanism for blood pressure regulation
91
what natriuretic peptides increase as atria and ventricles stretch?
increase in ANP and BNP
92
what natriuretic peptides should you look for in patients with heart failure
elevated ANP and BNP
93
effects of elevated ANP and BNP
1. decrease renin
2. direct vasodilation
3. increase in globular filtration rate
= naturesis and diuresis (excrete salt and water)
=decrease BP and blood volume
94
response by kidneys from hemorrage
secrete renin and angiotension to induce vasoconstriction
95
response by hormones released by the heart from hemorrage
decrease in ANP and BNP
96
neural response by baroreceptors from hemorrage
baroreceptors tell the sympathetic nervous system to increase firing of action potentials and increase HR
97
high blood pressure medications reduce the afterload or preload on the heart
afterload
