Respiratory

Respiratory



 Physiology

o The lungs are responsible for ventilation and gas exchange

o Gas exchange takes place in the alveoli

o Blood goes from RV to PA to lungs where it is oxygenated

o Oxygenated blood goes to LA, to LV, through aortic valve, out to body

o Compensate during pH imbalances

o Oxygen from lungs carried to tissues via hemoglobin

o If the lungs are damaged, the process is disrupted and the end result is

that the tissues receive less oxygen



 V/Q

o This confuses everyone, but it’s actually a very simple concept…you’ll be

saying “duh” by the end of this.

o V=ventilation--passage of air through the airways and into the alveoli of the

lungs.

o Q=perfusion (not p because that’s already used to stand for pressure)—this

refers to the blood flow to the lungs. After all, the goal of the lungs is to insert

O2, remove CO2 in the blood. If blood does not make it to the alveoli, this

process is greatly disrupted.

Matching—V and Q must match in order for the lungs to perform optimally



Pathophysiology of the Respiratory System

Acute Respiratory Failure

 It is just what it sounds like—an acute failure of the respiratory system.

 From what you’ve read above, you know that failure of the respiratory system either

can’t ventilate or isn’t well-perfused.

 There are two types of ARF: Type one=hypoxemia and normocapnia, Type

two=hypoxemia, hypercapnia.

 Obviously these patients will have acidosis—retaining huge amounts of CO2.

Causes

 Pulmonary emboli, trauma, COPD, near drowning, toxic inhalation, obstruction, pneumo,

etc.

Types

 Type I: V/Q mismatch, resulting in intrapulmonary shunting

o A moment to explain intrapulmonary shunting—When a V/Q mismatch exists,

it causes inadequately oxygenated blood to mix with oxygenated blood.

Therefore, the PaO2 will fall, due to a mixed-venous blood volume. Again, this is

the danger of a V/Q mismatch. Think about this though…which type of V/Q

mismatch that resulted in pulmonary shunting would NOT respond to O2 therapy,

and which would? Well, if the problem is a ventilation one, supplying extra O2

would help since there is still SOME ventilation. However, if the problem is that

there’s not enough perfusion, supplemental O2 will NOT HELP. Therefore, if

you have a patient who is not responding to O2 therapy, think low-perfusion

shunting!

 Type II: Alveolar hypoventilation with or without V/Q mismatch and shunting



Assessment

 Change in LOC, flushing/HA (high CO2), increased HR, RR, BP (compensation),

arrhythmias, CP, edema, cyanotic, pale, clammy



Management

 Need to fix V or Q, whichever one is screwed up.

 If it’s V, need PEEP to open the alveoli

 If Q, increase perfusion (sometimes tough to do) via medications

 Bronchodilators, sedation, intubation, fix ABGs

 Important to feed gut w/in 24 hours…if not have increased chance of pneumonia

 Good positioning—sick lung up. If both sick, R one goes down, HOB up, IS



ARDS

 Stands for acute respiratory distress syndrome

 A very nasty thing to have



Causes

 Aspiration, near-drowning, trauma, oxygen toxicity, sepsis, shock, etc.



Criteria

 Gas exchange is impeded

 Pulmonary edema (sound wet)

 PaO2/FiO2 is < 200…divide PaO2 by FiO2 (must have this to be ARDS!)

 The alveolar-capillary membrane becomes “leaky”—causes the pulmonary edema

 It is NON-CARDIAC pulmonary edema—best way to differentiate is through bronchial

sample (proteins and cells will be present in ARDS from leakage, not from pulmonary

edema from HF)

 Normal wedge pressure (again, non-cardiac)



Assessment

 Crackles galore

 SOB, anxiety

 “fluffy” exudates on CXR

 No peripheral edema (unless from some other ongoing problem)

 Inability to keep sats up (shunting)



Phases

 Exudative

o Happens 24 hours post insult

o Capillaries become leaky

o Pulmonary caps are damaged, send microthrombi

o Epithelial cells damaged

o Basically, the lungs start getting congested in this phase



 Fibrotic (weeks afterword)

o Granular deposits, leads to fibrosis

o Remodeling of lung tissue—alveoli damaged, pulmonary caps. Scarred

o Lungs now increasingly “stiff” with poor compliance



Management

 Oxygenation—generally intubation

 Inverse ratio ventilation (last ditch), normalizes the PaO2/FiO2 ratio

 Diuretics, broncodilators, enteral nutrition fast (pneumonia again)

 Prone positioning—a pain to do, but it is effective





Pulmonary Edema

 Patho—for whatever reason, fluid goes into lungs faster than it can be filtered out.

 Either from cardiac dysfunction, fluid volume overload, ARDS



Assessment

 SOB, crackles, high RR, ABG changes—resp. alkalosis to resp. acidosis

 Fatigue, change in LOC, frothy sputum (pink)

 Murmurs, dysrhythmias



Management

 Diuretics! Inotropes! (if cardiac)

 Treat underlying cause

 Oxygenation/ventilation

 Upright positioning



Pulmonary Embolism

 Venous thrombus mobilizes

 Lodges in PA

 Causes V/Q mismatch and shunting—increased dead space (plenty of ventilation but not

perfusion)



Assessment

 CP, SOB

 Cyanosis

 Hypoxemia, High PVR (there’s a big clot in there)

 Hemoptysis

 Petechiae

 Crackles

 Murmurs, ST changes

 Diagnosed using ABG and V/Q scan—most accurate



Management

 Support ventilation/oxygenation as needed

 Must dissolve the clot via heparin, thromolytics, coumadin, etc., or place filter

 Early enteral nutrition

 Bleeding precautions

 Prevention—SCDs, TEDs, check homan’s, etc.