Nurs 209 Respiratory/acid Base

Front 1

Which type of manifestion in the lungs would you see in each of the 2 types of emyphysema?

Back 1

In emphysema due to smoking or childhood resp. infections, or secondary smoke/air pollution, you would see: Centriacinar /Centrilobular, Respiratory bronchioles & then spreading out peripherally; Associated w/ chronic smoking; Affects upper ½ of lungs.
Then with inherited emyphysema you would see: Panacinar/Panlobular
Destroys entire alveolus. Deficiency of Enzyme α1 - antitrypsin. Affects lower lobes of lungs.

Front 2

What would be a few distingishing factors between chronic bronchitis and emphysema?

Back 2

In bronchitis there will be overwhelming fluid/mucous and enlargement of the goblet cells and lack of cilia; with emyphysema you would see irreversible enlargement of the airways, the alveolar walls have been attacked and destroyed exhitibing loss of recoil and breakdown of the alveolar walls leading to bolbus or bullae alveoli; with a subsequent loss of capillaries.Barrel chest – 1:1 ratio
Minimal wheezing (less mucous with than with bronchits;, Prolonged expiration, Pursed lip breathing
Thin body build; to much energy to breathe and not enough energy to eat. You would see possible cyanosis in bronchits because the airways are blocked with mucous. In emphysema you would see clubbing of the fingers.

Front 3

What does the alph 1 enzyme do?

Back 3

This enzyme is something we are normally born with that protects our alveolar walls. If you are born without it, you are set up for inherited emphysema.

Front 4

Why do we look at the anion gap? And how do we look at base excess?

Back 4

To differentiate metabolic acidosis. Base excess contains all bases and buffers not just bicarbonate, but if you have a deficit in bicarbonate, you'll have a deficit in base. and visa versa. Anion gap are electrolytes like sodium, potassium and subtract and whatever number they get to differentiate the cause of metabolic acidosis. It could be a loss of base or making too much acid. When someone has metabolic acidosis it could be due to their body is making too much acid or ate a lot of acid, they would have an elevated anion gap. But if someone loses a lot of base from diarrhea, or fistula, they would have metabolic acidosis, but the cause would be from a loss of ase bacause their anion gap would be normal.

Front 5

Part 1 of 2 parts: What is TV, FVC (IRV & ERV) FEV, VC, RV, FRC, TLC?

Back 5

Tidal volume is the normal amount of air on inspires and expires in a normal breath. TV will be decreased in severe resp. disease. FVC is the forced vital capacity of the lungs. It is a combination of the IRV and ERV together, Means I will inspire as much as I can and expire as much as I can, (we actually do this when we excercise heavy); FEV is Forced expiratory volume and is used as part of the FEV1 test. It will be decreased in persons with copd, obesity and ascites. Have a person take in a normal breath first and breathe out, then on the next breath take in as much as they can and then put their lips around the tube and blow as hard and as long as they can. This test will not only measure the amount of air they expired in the 1st second, but also the amount of air they were able to expire;

Front 6

What does FRC mean to different disease?

Back 6

FRC is Functional reserve capacity which will be a combination of our residual capacity and our ERV expiratory reserve volume (the volume that we expire if we force it out or when we are exercising. Otherwise known as the volume of air after a normal exhalation tha tis left in our lungs. These 2 combined make FRC and need to be high enough to keep alveoli open, 2300 ml.FRC should remain high enough to keep the alveoli open, 2300 ml-normal, but in atelectasis, pneumonia, pulmonary edema, and ARDS, the functional residual capacity (FRC) is reduced;
And In COPD and emphysema the FRC will be increased due to trapped air causing hyperinflation.

Front 7

How is ventilation, the movement of air in and out of lungs, regulated?

Back 7

Functioning Respiratory Control Center in _pons and medulla_____
Works w/ neurons respiratory muscles ANS innervates lungs
Receptors in lungs – have specific function; Epithelium & smooth muscle of airways; Located near alveolar capillary junctions
Chemoreceptors: important receptors to know! Detect gas exchange based on pH, PaO2 & PaCO2 Alters rate and depth of breathing.

Front 8

What is alveolar-capillary diffusion and what types of pathology could effect it?

Back 8

AC diffusion is the alveoli's incoming o2 diffusing across the the alvolar/capillary membrane into the blood. It naturally diffuses because of the concentration gradient-o2 is naturally higher in the alveoli and will follow the gradient theory where an area of higher concentration will flow into an area of lower concentration. In instances where there is pulmonary edema or fluid in the interstitial space between the membranes gets wider, there will be a longer, more difficult diffusion intereupting the ability of o2 to get into the blood. Also, if there is lack of surface area, there will be less diffusion of o2 because there is literally less areas available to pick up o2. Less surface area could be due to a portion of lung removed or emphysema, where the alveoli have widened and taken up space with bolus and there are less total alveoli being used, thus less surface area. Remember you would have less surface area 20 large alveoli then you would with 30 small alveoli....

Front 9

Explain perfusion

Back 9

Perfusion has to do with the blood that surrounds the alveoli that drops of CO2 and picks up O2 to take back to the heart and out to the tissues in the body. So unlike ventilation where we are talking about primarily the lungs, perfusion depends on the function in the lungs and the heart. They both need to be working hand in hand or the tissues will not get the o2 they need. It also depends on the blood itself, the hemoglobin, rbc, so perfusion is a lot more involved. In the lungs, however a problem in perfusion can be a mechanism called shunting. When an alveoli has become plugged or is no longer ventilating then the blood will SHUNT somewhere else. When there is no perfusion, perhaps due to heart problem or an embolus, but there is ventilation-this is called DEAD SPACE.

Front 10

In what diseases might you see a shunt?

Back 10

Atelectasis
Pulmonary edema
Pneumonia
Mucus plugs
ARDS

Front 11

What are the po2 and co2 levels in dead space? Which is high or low

Back 11

Pos2 would be high, but co2 would be low.

Front 12

What are the hallmark signs of hypercapnic caused acute resp failure syndrome? What are the hallmark signs of hypoxemic caused acute resp failure?

Back 12

Hypoventilation leading to hypercapnea: increase CO2
Ventilatory demand exceeds the supply: need more air; Respiratory:
Airflow obstruction & air trapping;
CNS-Suppress the respiratory drive
Medulla unable to respond
Chest Wall; Lung expansion is limited impair gas exchange; In
Neuromuscular: Weakened respiratory muscles impair gas exchange CO2.

In Hypoxemic acute rep. failure: – There is hypoxemia from impaired gas exchange; Alveolar ventilation-not enough O2;Diffusion is limited; VQ mismatching
Ventilation & perfusion
Intrapulmonary shunting: result of collapsed alveoli.

Front 13

Why is diffusion difficult in pulmonary edema?

Back 13

Because of the fluid that is built up between the alveoli and capillary membranes, diffusion and exchange is now more difficult because it has to travel a longer distance wading through the fluid.

Front 14

What can be another reason for difficult diffusion across the alveolar-capllary membranes besides fluid?

Back 14

Fibrosis or scarring as like in ARDS.

Front 15

Since all the following symptoms can present in variable degrees, (hypoxemia, hypercapnia, acidosis, HR, mild HTN(hypertension),it tells us that the body attempting to compensate, but it cannot tell us the severity of the problem, so what diagnostic tests do we turn to?

Back 15

ABG’s: Assess pH, O2: & CO2, CBC: (what is their hemoglobin, could be low), CXR (chest xray) is there atelectais, is there pneumonia?

Front 16

What would be the physiological criteria in order to be diagnosed with acute respiratory failure?

Back 16

Dx: ABG’s – RA (room air)
PaO2: 50-60 mm Hg or less
PaCO2: >50 mm Hg
(If CO2 retainer – pH < 7.35: copd patients will be less than this.
Usually < 7.25: probably more like this)

Front 17

Pa o2 55, on 4 L, increased the o2 to 100% non rebreather and now abg o2 is 50 that is refractory hypoxemia what does this indicate in disease?

Back 17

ARDS

Front 18

What causes ARDS?

Back 18

1) Shock: Hemorrhagic, Sepsis, Cardiogenic, or anaphylactic.
2) Inhalation injuries: Aspiration,
Smoke, toxic gas, Near drown, O2 toxicity; 3) Drug OD: Heroin, ETOH
4) Trauma: Head injury, burns
Pulmonary contusion, Multisystem, frx: fractures. 5) Pneumonia,
6) Embolism – air, fat 7) DIC: dicemminated intravascular coagulopathy, 8) Severe Pancreatitis
9) Cardiopulmonary bypass.

Front 19

What is the pathology of ARDS?

Back 19

Systemic inflammatory response (SIR) Inflammatory cellular responses & mediators damage the alveolar-capillary membrane:
Occurs w/in 90 min of SIR & w/in 24° of the initial insult. Result is massive inflammatory response by lungs. As the macrophages are released they go into the capillary bed and form microthrombi; also histamine, bradykinin and seratonin are released, which are increased and they increase the cap permeability and hence fluid will now shift out because of leaky caps and now fluid will sit between the alv/cap beds. As the fluid leaks, proteins also leak and starts spilling fluid into the actual alveoli, and as it collects in the alveoli it effects the o2/co2 exchange. Lung compliance will decrease as they start to fill with fluid, think about it, it's hard to fill up a balloon with water. This excess fluid starts to effect the type ii cells that produce surfactant, and so they won't be able to keep the alveoli open. In addition to this a hyaline membrane forms on the inside and outside of the alveoli that leads to fibrosis, and will all effect o2/co2 exchange.

Front 20

What happens during the fibrotic stage of ARDS?

Back 20

Pulmonary fibrosis; Cellular granulation & collagen deposits;
Alveoli enlarged & irregular;
Capillaries scarred & obliterated;
Lungs stiffen,pulm HTN, hypoxemia
Pulmonary vascular destruction & fibrosis; Remodeling occurs
Hmmm.. Is Remodeling a good thing? Not a good thing in the lungs, maybe in the kitchen.

Front 21

What is hyaline membrane disease?

Back 21

The newborns' ARDS

Front 22

What can be all the clinical manifestations of ARDS?

Back 22

Dyspnea, tachypnea; Resp distress
Retractions, use of acccessory muscles; Cyanosis; Breath sounds
Initially clear, diminshed, rales & rhonchi; Agitated, confused; O2, hypoxemia, Hypocapnia – early;
Hypercapnia – late; Lactic acidosis – late; CXR: Chest xray; Edema not evident until 30% fluid; Diffuse infiltrates; Widespread “whiteout".

Front 23

What are the unifying signs found in obstructive resp. disease?

Back 23

Major symptom of obstructive pulmonary disease is DYPNEA and the unifying sign is WHEEZING: means fluid is in the lungs.
Individuals have INCREASED WORK OF BREATHING, V/Q mismatching, and a DECREASED FORCED EXPIRATORY VOLUME.

Front 24

Why is asthma not considered a copd disease?

Back 24

Because it is usally more acute, more intermittent, and can be found in children.

Front 25

What is unique to the mucous in copd patients?

Back 25

Goblet cells enlarge from inflammation. and there is a large amount of mucous. This is partly due to the absent cilia that normally remove mucous.

Front 26

What would be the unifying symptoms of Chronic Obstructive Pulmonary Disease (not just obstructive, but chronic). Remember that COPD is an umbrella for 2 diseases.

Back 26

WBC’s invade the lung and release mediators, brady, sero, and hist and invade the epithelium of central airways, which contributes to edema.
Mucous secreting glands enlarge
in goblet cells, which leads to excessive mucous secretion & ciliary dysfunction: usually ciliary brings up the mucous. CHRONIC inflammation of peripheral airways means repeated damage & repair: not good! Results in destruction of lung parenchyema ( structures within the lungs); Leads to pulmonary hyperinflation & impaired gas exchange. Vascular changes: thickened vessel walls and so pulmonary hypertension develops.
Acute Cor Pulmonale; right sided failure of the heart, because of the increased pulmonary resistance putting more pressure on the heart.
Cor Pulmonale>>Defect w/ R vent(the chamber that pumps blood into the lungs and it has to overcome the pressure of the lungs. The heart gets overstretched and can’t go back to its normal size).

Front 27

What is important to remember to distingusih about the bronchitis and emphysema

Back 27

That the inflammation in chronic bronchitis is just as it's name implies, the inflammation is especially targeting the bronchioles, and with emphysema it is attacking the alveoli.

Front 28

So what are the clinical manifestations of chronic bronchitis?

Back 28

Chain of events: Mucous glands hypertrophy in response to tobacco smoke. Excessive mucous production in bronchial tree; Excessive sputum production results; Tobacco smoke damages cilia; Cough occurs to clear excess sputum; Chronic inflammation swelling of bronchial walls
Excessive secretions can block airways. Dx made: chronic cough & sputum production on daily basis
Minimum of 3 months/year
Not less than 2 consecutive years;
Symptoms: Chronic, productive cough. Often w/ purulent sputum
Progressive Dyspnea w/ exertion
Continuum – most won’t seek assist until troublesome; Disease is well advanced DOE (dypnea on exertion)
Intermittent wheezing & crackles – auscultation;Prolonged expiratory phase; Hypoxemia, hypercapnia, cyanosis. R/t bronchial mucous & obstructed ventilation; FEV1, Prolonged FET (forced expiratory time).

Front 29

What is the etiology and pathophysiology of chronic bronchitis?

Back 29

ETIOLOGY: Cigarette smoking
Repeated infections of airways
Physical or chemical irritants; PATHOPHYSIOLOGY: Inspired irritants caused >>>>inflammation of the airways involving Neutrophils, macrophages, T lymphocytes that release chemical mediators leading to lots of fluid. >>Leads to over- whelming bronchial edema>>>which narrows airway & obstructs airflow >>>Hyperplasia of mucus glands and goblet cells>>>destruction of cilia>>>Mucus is thick and tenacious and can’t be cleared r/t impaired ciliary function>>>Increases susceptibility to infection and injury; Ciliated epithelium allows fine particles to enter airway; Defense mechanisms not effective;
Bronchial wall thickens fibrosis
evenutally all airways will be effected.Initially affects only larger bronchi, but eventually all airways involved. Airways collapse in early expiration, blocked by mucus, and air is trapped in distal portion of the tract>>>Leads to ventilation/ perfusion mismatch>>>Hypoxemia occurs>>>Air trapping prevents respiratory muscles from functioning efficiently>>>Hypoventilation and hypercapnia.

Front 30

What is the time frame needed in order to diagnose bronchitis?

Back 30

Dx made: chronic cough & sputum production on daily basis
Minimum of 3 months/year
Not less than 2 consecutive years

Front 31

What is the pathophysiology and eitiology of emphysema?

Back 31

Attacks the alveolar walls & elastic tissue support; Decrease in surface area for gas exchange; Obstruction results from changes in lung tissue;
Resistance of airways is increased.
Increased resistance to pulm blood flow r/t destruction of alveolar walls w/ a subsequent loss of capillaries; the body won’t want to perfuse an unventilated avleoli; Alveolar hypo- ventilation hypercapnia, hypoxia, arterial hypoxemia;Attacks the alveolar walls & elastic tissue support; Decrease in surface area for gas exchange; Obstruction results from changes in lung tissue
Resistance of airways is resistance to pulm blood flow r/t destruction of alveolar walls w/ a subsequent loss of capillaries; the body won’t want to perfuse an unventilated avleoli.
Alveolar hypoventilation hyper- capnia, hypoxia, arterial hypoxemia; Major cause is cigarette smoking
Smoking impairs alveolar function
Smoke triggers the inflammatory response: Neutrophils & macrophages release proteolytic enzymes that destroy the elastin in the lungs (because of inflammation) loss of recoil. Major mechanism is loss of elastic recoil: breakdown of interntal walls. Air trapping in distal alveoli distended air sacs; Loss of alveolar walls & air trapping bullae: bolbus appearance.

Front 32

What are the clinical manifestations of emphysema?

Back 32

Progressive Exertional Dyspnea
Dyspnea at rest; Barrel chest – 1:1 ratio; Minimal wheezing
Prolonged expiration; Pursed lip breathing;Thin body build; to much energy to breathe and not enough energy to eat.; Hypoxemia – t/o disease; Hypercapnia – as disease progresses; Polycythemia & Cor pulmonale; Late in the progression of the disease; FEV1, Prolonged FETime > 6 seconds

Front 33

Part 2: VC, RV, FRC, TLC?

Back 33

VC is the amount of air the lungs can hold, but not including the residual volume, said another way it is Max volume of air exhaled from the point of max inspiration (vital capacity). VC is decreased in atelectasis, pneumonia, but is increased in copd. RV, (which is the air that is never expired from our lungs, but basically keeps the alveoli from collapsing); RV will be increased in persons with copd due to hyperinflation and compliance. FRC is a measurement of not only the ERV or air that we hold in reserve expiration for times when we exercise, but also the residual volume (the air we never use, but is there holding things open), FRC is a combined total of these 2: RV and ERV together. The TLC is the total amount of air the person could possibly hold in their lungs including residual volume.

Front 34

Hydrogen ions circulate around our body in certain forms. What are they?

Back 34

H+ ions Circulate throughout body as: 1) Volatile Acids: carbonic acid
Carbonic Acid - H2CO3 or
broken down to H2O + CO2

and 2) Nonvolatile Acid - fixed acid
metabolic acids in our body fluids
Lactic Acid, Pyruvic Acid

Front 35

What is the ratio of Carbonic acid to bicarbonate?

Back 35

1 carbonic acid to 20 bicarbonates keeps things in balance of acid base balance.

Front 36

What is PaO2? What is normal PaO2? What are the different numbers values that determine, mild, moderate and severe hypoxemia?

Back 36

PaO2 is the amt of O2 dissolved in blood. The normal value for PaO2 =
80-100 mm Hg. This value can be affected by age & altitude. If a person has < 80 mm Hg to 60 = mild hypoxemia; If a person has < 60 mm Hg to 40 = moderate hypoxemia; and if a person has < 40 mm Hg = severe hypoxemia.

Front 37

Explain Base Excess/ and Deficit

Back 37

Base excess/ deficit is a measurement of total buffers in body. It reflects metabolic disturbance. The normal range for base should be-2 mEq/liter to +2 mEq/liter. Base excess will go into the same direction as the bicarbonate. So if things become alkalitic and you have a bicarbonate of 30 you will have a maybe a +9 of base excess. If you have bicarbonate of 10 indicating acidosis, you may have a base deficit of -16.

Front 38

Anion Gap: What is it used for and what does it indicate?

Back 38

The anion gap is used for indicating what is causing the diagnosis of metabolic acidosis (only). Normal range is 8mEq -12 mEq. So if a person starts to go higher than this value then their metabolic acidosis is due to too much acid in the body and not to loss of base. If the person has a normal anion gap, and they have metabolic acidosis then then it is probably caused by a loss of base (probably from vomiting or diarrhea.)