Quiz 1 Flashcards
1
Q
the inability of the heart to pump blood at a rate that is proportionate with the requirements of the metabolizing tissues or can only do so from an elevated filling pressure
A
Heart Failure
2
Q
You can have LVD but not have heart failure IF…
A
you can still meet the demands of the heart
3
Q
Compensatory mechanisms
A
natriuretic peptides
Frank-Starling mechanism
Myocardial hypertrophy
sympathetic reflexes
renin-angiotensin-aldosterone mechanism
-all of these function in maintaining the cardiac output in a failing heart
4
Q
Frank- Starling compensatory mechanisms
A
increased EDV
only works to a certain point
the more you put in, the more you get out
5
Q
Myocardial hypertrophy compensatory mechanism
A
gradual change of the muscle cells and fibrous tissues that undergo hypertrophy
primary response is to generate an extra pump to go against the resistance
need more oxygen for more muscle but there is less wall stress with more muscle
*long term
6
Q
Renin-angiotensin-aldosterone compensatory mechanism
A
The kidney produces renin which creates angiotensin to produce angiotensin II from ACE. Aldosterone is produced with helps with salt and water retention. This then increases the vascular volume therefore increasing venous return
7
Q
Sympathetic reflexes compensatory mechanism
A
There is a high HR with heart failure which creates a ramped up sympathetic nervous system
These reflexes increase HR and contractility to improve cardiac output
*short term
8
Q
Natriuretic peptides compensatory mechanism
A
counters overactivity of compensatory mechanisms
produced by the heart muscle cells in response to stretch
promotes excretion of Na+, water and potassium
inhibits aldosterone
acts as an antagonist for Ang II and inhibits NE therefore decreasing the volume of the heart to result in less stress
9
Q
Causes of Heart Failure
A
cardiomyopathies myocarditis coronary insufficiency myocardial infarction stenotic valces regurgitant valves congenital heart disease systemic or pulmonary HTN excessive intravenous fluid administration thyrotoxicosis severe anemia
10
Q
Normal symmetric hypertrophy
A
thickness of wall increases in proportion to the wall of the chamber
11
Q
Concentric hypertrophy
A
disproportionate increase in wall thickness
12
Q
Eccentric hypertrophy
A
disproportionate decrease in wall thickness
as the wall thins the chamber gets bigger
there is not enough pumping power with a stretched out wall therefore as wall stress increases so does oxygen demand
13
Q
high output
A
usually caused by anemia
the heart keeps working and working but is not meeting the demands because oxygen content of the blood is insufficient
14
Q
low output
A
more common classification
not generating sufficeint CO
15
Q
systolic
A
more common classification
blood moving out
16
Q
diastolic
A
blood filling
17
Q
right sided heart failure
A
pressure backs up into the right atrium so that forces move into the systemic venous system
18
Q
right sided HF symptoms
A
fatigue dependent edema (localized in a dependent area) distention of the jugular veins liver engorgement ascites (fluid in peridinium accumulates) loss of appetite cyanosis elevation in peripheral venous pressure
19
Q
Left sided heart failure
A
more common
can cause right sided HF
blood backs up into the lungs causing pulmonary edema
20
Q
Left sided HF symptoms
A
symptoms related to congestive HF
exertional dyspnea
orthopnea ( difficulty breathing while lying down)
paroxysmal nocturnal dyspnea (SOB suddenly at night)
cough
cyanosis
fatigue
elevation in pulmonary capillary wedge pressure
21
Q
common signs and symptoms of HF
A
fatigue fluid retention and edema pulmonary symptoms altered exercise tolerance cachexia (muscle wasting) malnutrition cyanosis (impaired oxygen delivery)
22
Q
Treatment
A
turns down the influence of compensatory mechanisms that can worsen conditions
diuretics, ACE inhibitors/ARBs and Beta blockers are most popular and all lower BP
23
Q
Diuretics
A
get rid of excess fluid (loop-diuretics) therefore decreasing stress on the heart
24
Q
ACE inhibitiors/ARBs
A
produce less vasoconstriction and less fluid retention therefore decreasing stress and vascular volume of the heart
25
Beta blockers
decrease contractility of the heart by lowering sympathetic activity and concentration of NE to normalize cardiac function
metoprolol
26
digitalis (Digoxin)
less common
an antiarryhtmic taken by mouth to increase contractility and Ca2+
diminishes symptoms and creates better QOL
27
Aortic balloon pump
INFLATED to increased the driving pressure of blood flow during DIASTOLE
helium is sucked out to create a space and decrease demand in the artery during SYSTOLE
28
Impella
temporary
| takes blood from one end and pumps it into another end
29
Thoratec HeartMate II LVAD
semi-permanent
pulls blood out of LV and puts it back in aorta so that LV doesn't do much work
alternative to transplant
30
circulatory shock
failure of circulation to maintain adequate perfusion of vital organs. results in impairment in O2
patients tend to be hypotensive and tachycardic
there is a shift from aerobic----> anaerobic metabolism
exhibit increased levels of lactic acid in the blood
31
circulatory shock- cardiogenic
impaired O2 delivery, contractility and CO
direct extension of heart failure
most commonly caused by MI
characteristic trait of low BP
32
circulatory shock- hypovolemic
diminished blood volume so that there is not enough to deliver adequate oxygen
can be caused by fluid shifts, burn injuries, hemorrhage or severe dehydration
33
circulatory shock- obstructive
not common
results from mechanical block of blood flow through the central circulation
there is impairment in heart filling (preload)
most frequent cause is pulmonary embolism
results in elevated right heart pressure
34
circulatory shock- vasodilatory (distributive)
there is so much vasodilation occurring that pressure gradients are decreased which results in anaphylatic shock
35
signs and symptoms of circulatory shock
```
cool
clammy (diaphoretic)
cyanotic
poor renal output
altered mental state (confused, unresponsive)
```
36
mild hypovolemic shock
slight tachycardia
slight decrease in BP
15-25% volume loss
37
moderate hypovolemic shock
HR 100-120
SBP 90-100
pallor, oliguria (not making enough urine)
25-35% volume loss
38
severe hypovolemic shock
HR >120
| SBP
39
septic shock
```
most common type of vasodilatory shock
systemic vascular resistance problem
severe infection with low BP
linked to strong vasodilatory response
40% mortality
gram-negative bacteremia which is bacteria in the blood that initiates an inflammatory response
```
40
complications of shock
adult respiratory distress syndrome (ARDS)
-form of pulmonary edema
acute renal failure
gastrointestinal complications
disseminated intravascular coagulation (DIC)
multiple organ dysfunction syndrome (MODS)
41
general functions of the respiratory system
speaking
brings in O2
gets CO2 out
helps to regulate blood pH level
42
Which branches make up the Conducting Zone?
trachea, bronchi, bronchioles, terminal bronchioles
43
role of the conducting zone
takes air from the outside and brings it into the body
air is warmed to body temp and humidified
gas is filtered and cleaned via secreted mucus
NO gas exchange occurs here
ciliated epithelial tissue makes up this zone
44
role of respiratory zone
gas exchange with huge surface area
45
What occurs as you go down the branches of the respiratory system?
the amplification of division and number of structures gives a large surface area for gas exchange to occur
46
What important purpose do the bronchioles serve?
the control resistance and air flow through the lungs
47
difference between bronchi and bronchioles
bronchi have cartilaginous plates which give them structure
| bronchioles do not which makes them much more susceptible to injury or disease
48
Type I alveolar cells
squamous epithelium involved in the process of gas exchange between the alveoli and blood.
cover 95% of alveoli surface
49
Type II alveolar cells
Their function is of major importance in the secretion of pulmonary surfactant, which decreases the surface tension within the alveoli.
capable of cellular division
they are fewer in number
50
structure of alveoli
"cluster of soap bubbles"
they share walls and have interconnectedness with adjacent alveoli
-this can help with pressure gradient and gas distribution
51
parietal pleura
lines the inside of the rib cage
52
visceral pleura
in direct contact with the lungs
53
intrapleural space
has negative pressure which acts as a suction cup and is able to keep your lungs stuck to your rib cage
if there is a hole or cute here then your lung can collapse
54
Palv
pressure in the alveoli
55
Patm
atmospheric pressure
this changes with location
it is the reference point. Patm = 0
56
For air to move from the room into the alveoli....
Palv must be lesser than the room
57
For there to be no air movement...
Palv=Patm
58
Pip
pressure of the interpleural fluid
keeps the alveoli inflated
always negative
59
Transpulmonary pressure
Palv -- Pip
pressure difference across the wall of the alveoli
the bigger the difference the greater the alveoli expansion
60
What generates pressure changes during a normal respiratory cycle?
muscle activity
61
What happens when Palv drops below Patm?
inspiration
62
What happens when Palv > Patm as we breathe?
exhalation
63
Palv = Patm
no change in breathing
64
during inhalation.....
Pip becomes more negative while the transpulmonary Pressure increases therefore allowing alveoli to expand
65
during exhalation...
Pip becomes less negative
66
Diaphragm and inhalation
as the it contracts it drops down and increases the thoracic volume while decreasing the pressure creating a pressure gradient for air to move in
Pip decreases and becomes more negative while the transpulmonary pressure increases to increase alveoli
67
relaxation of the diaphragm causes?
transpulmonary pressure to decrease and the size of the alveoli to decrease
68
Role of pulmonary surfactant
produced by Type II alveolar cells
- reduces surface tension of water molecules in alveoli
- makes them more compliant; ease of lung inflation
- helps keep alveoli dry
- prevents pulmonary edema
69
Describe what it means that our lungs are compliant
This means that they have ease with stretching and don't need to work hard to expand alveoli
- the ease of inflating
-determined by the elastic properties
of the lung, its water content, and surface tension
70
What decreases lung compliancy?
diminished by conditions that reduce the natural
elasticity of the lung, increase the surface tension in
the alveoli, or impair the flexibility of the thoracic cage
71
A lung that is more compliant loses what ability?
loses the ability to recoil; return to its original shape
| This is because the overstretched tissues are easier to inflate but more difficult to deflate
72
What makes up pulmonary surfactant?
mixture of phospholipids, neutral lipids, and proteins made by Type II alveolar cells
developed in the 26-27th week of gestation which is why many premature babies have pulmonary issues since their surfactant has not been fully produced
73
Why do we encourage our bed-ridden patients to cough?
deep breathe enhances the spreading
of surfactant, allowing for a more even distribution
of ventilation and prevention of atelectasis
74
What is atelectasis?
partial or complete collapse of a lung
75
During what action is there more resistance of the airways?
During exhalation
-This is because elastic-type fibers connect the outside of the airways to the surrounding lung tissues. As a result, these airways are pulled open as the lungs expand during inspiration, and they become narrower as the lungs deflate
during expiration
76
What happens to the airway radius during inspiration?
It is greater therefore resistance to flow is decreased
77
Resistance to flow is inversely related to....
airway raidus
78
What is the effect of exercise on airway resistance?
it significantly increases it with forced expiration
79
What happens to Pip during forced exhalation (coughing)
it becomes positive and dynamic compression of small airways occurs
80
What happens to the airway radius during exhalation?
airway radius is less therefore resistance to flow is increased
81
What happens to the lungs if Pip exceeds Palv greatly?
It can cause the lungs to collapse
palv --- PIP = -- Tp
compression
82
Airway diameter is narrowed as a result of?
a negative transpulmonary pressure
83
Airway diameter is greater at...
larger lung volumes
84
Higher expiatory flow rates can be achieved with?
higher lung volume
85
What factors increase resistance to flow?
```
bronchiolar constriction
-caused by parasympathetic stimulation
histamine
-allergic response
decreased PCO2 levels
expiration
```
86
What factors give less airway resistance?
```
brochiolar dilation
-caused by sympathetic stimulation
epinephrine and analogs
-B2 stimulation
increased Pco2 levels
inspiration
```
87
What does high PO2 mean?
it means good ventilation locally so arterioles DILATE to increase local blood flow
88
What does low PO2 mean?
it means poor ventilation locally so arterioles CONSTRICT to divert blood to areas of the lung that are well ventilated
89
Ventilation Perfusion Ratio (V/Q)
a measurement used to assess the efficiency "V" – ventilation – the air that reaches the alveoli and "Q" – perfusion – the blood that reaches the alveoli.
Our goal is to maximize this
90
How can you maximize V/Q?
........?
91
Tidal Volume
500 mL
| the amount of air that moves into and out of the lungs during a normal breath
92
Inspiratory Reserve Volume
2000 mL
maximum amount of air that
can be inspired in excess of the normal TV
93
Expiratory Reserve Volume
1200 mL
maximum amount that can be exhaled in excess of
the normal TV
94
Residual Volume
1200 mL
| air that remains in the lungs after forced expiration
95
Total Lung Capacity
4900 mL
TV +RV + ERV + IRV
sum of all the volumes in the lungs
96
Functional Residual Capacity
2400 mL
RV + ERV
it is the volume of air that remains in the lungs at the end of normal expiration
97
Vital Capacity
3700 mL
IRV +TV +ERV
amount of air that can be exhaled from the point of maximal inspiration
98
Why are these lung values greater in men and taller individuals?
these populations have greater lung volumes and capacities which is why they have higher values
99
What is total minute volume?
the amount of air exchanged in one minute
| Ve = Vtidal x f (respiratory rate)
100
What is Valv?
volume of gas that can be used to get O2 and lose CO2
101
Why is shallow breathing fatiguing?
You must breathe faster to maintain Valv so it is less efficient due to the constant dead space volume
There is reduced oxygen and blood circulation in the lungs with shallow breathing
102
Flow-Volume Loop
air flow rate vs. lung volume during a forced expiratory maneuver
103
If there is ventilation without perfusion....
V/0
increases dead space
gas exchange is impaired with lack of blood flow
you end up being ventilated with no gas exchange
104
If there is perfusion without ventilation....
0/Q
shunting
alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region
105
Obstructive airway disease
persons usually find it less difficult to inflate their
lungs but expend more energy in moving air through the
airways. As a result, these persons tend to take deeper
breaths and breathe at a slower rate to achieve their oxygen needs
106
persons with stiff and noncompliant lungs
expansion of the lungs is difficult for persons
with stiff and noncompliant lungs, they usually find
it easier to breathe if they keep their TV low and breathe
at a more rapid rate to achieve their minute volume
107
What is dead space?
the volume of gas that fills conducting airways
does not participate in gas exchange
150 mL
108
What happens with hyperventilation?
it increases PO2 in the alveoli
it decreases PCO2 in the alveoli
-you breathe deeper and more rapidly
109
Partial pressures of deoxygenated venous blood
lower pO2 and higher pCO2
110
Components of hypoventilation
slow breathing
CO2 accumulates in the alveoli while O2 is removed
changes seen in arterial blood
PO2 is lower while PCO2 is higher
111
factors affecting gas exchange at the lung
```
concentration difference
surface area
diffusion distance
altitude
supplemental oxygen
```
112
Which diseases have increased diffusion distance?
pulmonary edema and fibrosis of the lungs
| -this slows down diffusion
113
Levels of the lung and V/Q
upper lung = more ventilation
middle lung = V=Q
lower lung= more perfusion
114
the oxygen-Hb dissociation curve
shows how much O2 has Hb bound to it
| the goal is to keep patients in the plateau region where they are well saturated
115
Shifts in the O2-Hb dissociation curve
with exercise the muscles produce more CO2, there is an increase in temperature and RBC 2,3 di-PG
There is a shift to the right as things increase but there is lower Hb saturation
116
lower Hb saturation means?
more readily to let of O2
117
Left shifts in the O2-Hb curve
increased saturation so Hb is less likely to give up O2
118
Effect of anemia on the O2-Hb cuve
someone with anemia does not have enough Hb therefore they have low oxygen levels
