Download Cardio-11-09-98

Cardio Notes
11/9/98
Know questions: 50, 52, 54, 60-65, 67,68,70,75-79, 81-88
VENTILATION RATE (Breaths per minute)
I.
II.
Things that STIMULATE ventilation rate
A. Chemoreceptors
1. Chemoreceptors set off by PaO2. – (normal PaO2 = 95 mmHG)
If PaO2 <60, these receptors kick in. These receptors are the carotid and aortic bodies. They are
sensitive to O2 levels. They are PERIPHERAL chemoreceptors.
2. Chemoreceptors set off by pH – (normal ph – 7.35 – 7.45)
If pH < 7.35, these receptors act to increase the breath per minute.
If pH < 7.30, Kussmaul breathing begins, deep, gasping breaths ( as in diabetic keto acidosis).
3. Chemoreceptors set off by PaCO2 – (normal PaCO2 = 45mmHG)
These are central receptors. In hypercapnea, there’s too much CO2 in the system. If this
continues for more than 6 weeks, chronic hypercapnea sets in. The patient, then, can no longer
blow off CO2. Thus the V/Q balance is off. Increasing PaCO2 causes a decrease in pH. The body
compensates, as stated above, by increasing the breaths per minute. This doesn’t fix the problem
in conditions such as COPD. So the pt. retains more bicarbonate (HCO3-) to buffer the pH
decrease. (normal HCO3- is 21 m eq) In these cases, the pt. can get get up to a nd greater than
30 m eq. With this in place, the patient’s pH become normal again. So now, the central
chemoreceptors think that everything is just great. Now, the patient must rely upon the
peripheral chemoreceptors to tell the brain that there is a problem with hypoxemia and
hypercapnea. The aortic and carotid bodies, the “hypoxic drive”, are all the body has left to rely
on for data. If as this point, we give the pt. O2, the peripheral chemoreceptors think everything is
ok. They stop prompting to patient to breath more and this can become fatal.
B. Mechanoreceptors
When these are stimulated, there is an increase in the breaths per minute (ventalatory rate). In a
healthy patient, this results in a decrease of CO2 and an increase in O2.
1. Irritant receptors – the stimulation of these receptors causes an increase in breaths per minute,
laryngeal constriction and constriction of the glottis. This causes “barking” sounds as the person
breathes (stridor).
2. J receptors– the stimulation of these receptors causes an increase in breaths per minute and
vasoconstriction of peripheral arteries. (This is why exercise is difficult for asthmatics, they fatigue
more easily.)
3. Deflation receptors – the stimulation of these receptors causes an increase in breaths per minute but
how they do this is a mystery. There is no known nerve that causes this. In short, these receptors
cause an increase in breaths per minute if part of the lung collapses.
C. Dyspnea
A feeling of shortness of breath. To compensate, the pt. increases his breath per minute. This is from
proprioceptive input.
1. J receptors – in lungs
2. Costovertebral joints
3. Diaphragm spindles – (Factoid: when the lungs are hyperinflated, as in emphysema, the diaphragm is
depressed.)
4. Intercostal spindles
Aside: the Thoracic Pump, a technique of pressing on the thoracic cage, gives a great sense of relief to
asthmatics and COPD patients. It increases lymph flow and improves movement thus decreasing the
feeling of shortness of breath. It also helps associated sympathetic problems.
D. Decreased compliance, Increased recoil
If the lungs have decreased compliance and increased recoil, as in all restrictive lung diseases, the result is
decreased airway resistance (Raw). The airways get bigger. This causes an increase in breaths per minute.
This occurs in pneumonia. The pt. has a fever and increased breath per minute. Normally, the I:E ratio (time
of inspiration to time of expiration) is 1:2 due to the active nature of inspiration and the passive nature of
expiration. As the rate of breathing increases, the I:E ratio becomes 1:1. The time of expiration is lowered due
to a decrease in airway resistance and an increase in recoil.
Things that INHIBIT the ventilation rate
A. Hering-Breuer reflex – this is to prevent over-inflation. This is a reflex from the smooth muscle. This is the only
reflex that decreases the breath per minute. When a part of the lung collapses (as in pneumothorax or
atelectasis) the smooth muscle is compromised no stop can occur as it does in normal tissue to stop
overinflation.
B. Increased compliance and decreased recoil – This increases airway resistance (Raw). The I:E ratio become
1:4. It takes a great deal of energy to expire. Some people respond by increasing their breaths per minute,
some respond by decreasing their breaths per minute.
Increased breaths per minute Decreased breaths per minute
Pink puffers
Blue bloaters
Thin, wasting away
Bloated, fatter
END OF OUTLINE
Discussion of Bullae and specimen from the gross lab. In emphysema, bullae may develop. These are blisters of air on
the surface of the lung. A fistula forms and then becomes a blister, of bulla. If this bulla ruptures, air can leak into the
potential space between the parietal and visceral pleura. When this happens, the lung collapses. This in the most
common cause of lung collapse in pts. with emphysema. Blister upon the lungs also can occur in people with no apparent
lung problems, especially tall, thin males between 20 and 30 years old. Gravity pulls the lungs down and they can get
blisters of the lungs. These are called BLEBS. If these rupture, the lung can collapse very suddenly. Within minutes, the
pt. is dyspneic and the more they breathe in, the more air gets into the lung cavity space. There is a valve here that lets
air out into the pleural cavity, but doesn’t allow the air back into the lungs. This air stays in the space and begins to press
on the lung and the heart as the amount of air in the cavity grows. The lung collapses further. The air can go as far as
impeding venous return to the heart. This can cause death in 1.5 hours. Treatment in the emergency room begins with a
chest tube near the sternum. If this doesn’t work, they insert the tube between two ribs and suck out the air that is in the
chest cavity. Normally, these blisters aren’t huge. This condition is called “spontaneous pneumothorax”. Upon
auscultation, this area of pneumothorax is a “silent unit”. It is silent – there is neither blood nor air-filled lung in this area.
V/Q IMBALANCE:
Healthy people have a normal V/Q imbalance. Splitting the lungs into three horizontal sections, Zone 1 is the top section,
Zone 2, the middle section, and Zone 3 is the bottom section at the base of the lungs.
Zone 1 – Increased Ventilation
Decreased perfusion
V/Q increases – V/Q = 3.3/1.5
Zone 2 – Ventilation = perfusion
Zone 3 – Decreased ventilation
Increased perfusion
V/Q decreases – V/Q = 1.5/3.5
The objective is to maintain a 1:1 V/Q balance OVERALL in the lungs. This works out to be about 4.8/5.0. This is good!
Normal V/Q = .80. If there is damage to the lung tissue, this throws everything off.
4 SCENERIOS FOR V/Q:
1.) Normal - V is good, Q is good.
2.) Dead space unit – increased V, decreased Q. There is wasted ventilation.
Dead space:
Anatomical dead space – the conducting zone (in which no gas exchange occurs). This includes
the trachea through the terminal bronchiole. This is normally about 150 mL in the adult, about
1/3rd of tidal volume.
Alveolar dead space – wasted air. The air is there, but is doesn’t participate in
respiration because of decreased perfusion.
Anatomical dead space + alveolar dead space = physiological dead space. This should be equal to the
anatomical dead space in a healthy person.
3.) Shunt unit. Decreased ventilation, normal perfusion. Here, there is wasted Q. This has nothing to do with dead space.
Shunted blood is blood that traveled through the lungs and is still rich in CO2 and poor in O2. No, or very little, gas
exchange took place. Decreased V/Q here. All pulmonary diseases fall into this category. The ventilation is dramatically
decreased, but there is still plenty of perfusion. It is normal to have 2-5% of the blood be shunted blood.)
4.) Silent unit – decreased ventilation, decreased perfusion. Here, there is collapse. For example, pneumothorax.
Condition/Cause of V/Q imbalance:
1. increased physiological dead space
2. normal lung apex – upright
3. restrictive pulmonary disease
4. obstructive lung disease
5. alveolar dilitation
Decreased V/Q
Increased V/Q
X
X
X
X
X
6. lung apex – supine
X
(In a diseased state, the pt. would experience orthopnea.)
7. pulmonary emboli
8. chronic pulmonary hypertension:
due to emphysema
X
due to left sided heart failure
9. increased Raw (airway resistance)
X
10. congestive hearth failure
11. decreased compliance
X
12. atelectasis
X
13. polio
X
14. vagal syncope
15. pulmonary fibrosis
X
16. ventricular fibrillation
17. morphine overdose
X
(this shuts down the respiratory centers)
18. asthma
X
19. pulmonary edema
X
20. decrease in surfactant
X
(as in infantile distress syndrome, or hyaline membrane disease)
X
X
X
X
X
When there is alveolar dilitation, this decreases V/Q. In bronchiectasis, the alveolus is so large, that only those air O2
molecules that touch the alveolar wall will be eligible for gas exchange. The others, that vast majority, will not have a
chance as gas exchange. (Remember, all lung diseases/condition decrease V/Q.)