Respiratory Failure

Atelectasis

not a causal factor in post-operative fever (Chest 2011;140(2):418)

 

Respiratory Failure

Type I-hypoxemic, PaO2<60

Type II-hypercapneic w/wo hypoxemia, PaCO2>50

 

Mechanisms of Hypoxemia

1. Inadequate PAO2
   • Alveolar Hypoventilation
   • Decreased FiO2
2. V/Q Mismatch
3. Shunt (Will not improve with O2)
   • Intrapulmonary (Pneumonia, ARDS)
   • Intracardiac
4. Diffusion Abnormality
5. Low SvO2

PAO2=FiO2(PB-PH2O) – PaCO2/R

R=.8

 

Hypercapnea

VT=VA+VD (Alveolar/Deadspace)

PaCO2=PACO2 in normal lungs

 

Increased CO2 production (hypermetabolic states)

Decreased Alveolar ventilation/Increased deadspace ventilation

Decreased Tidal Volume

 

Reabsorbtion atelectasis and loss of hypoxic pulmonary vasoconstriction may actually cause hypoxemia to get worse in the presence of high fiO2 and shunt.

 

article on the mechanisms of hypoxemia (intensive care medicine 2005;31:1017-1019)

 

 

 

Decreased PaO2 can actually lower respiratory drive in the critically ill, studies done in patients with cardiogenic shock.

Primary neurologic problems can result in decreased respiratory drive.  these include AML, spinal cord injuries, guillain-barre, and muscular disorders.

Respiratory muscle fatigue from COPD/Asthma, ARDS, etc.

 

Increased production in sepsis, hypothermia, salicilates,

Increased deadspace ventilation

Hypercapnia can decrease respiratory drive.

Non-pulmonary Causes of Respiratory Failure

Obesity-hypoventilation Syndrome-“Pickwickian”, obesity, sleep apnea, respiratory muscle weakness

Immunologic Lung Disease

Goodpasture’s

Antibasement membrane

give immunosuppression and steroids

Wegener’s

Upper airway involvement

SLE

pneumonitis gets high dose steroids and cyclophosphamide

Rheumatoid Arthritis

interstitial fibrosis or BOOP

Bronchiolitis Obliterans with Organizing Pneumonia (BOOP)

acute illness with respiratory failure

cough, dyspnea, flu-like syndrome

restrictive lung pathology

prednisone 1 mg/kg/day

Idiopathic Pulmonary Fibrosis

smokers are at the highest risk

interstitial pneumonitis

restrictive pathophysiology

use low volumes and high rates

increased risk of lung cancer and cardiac ischemia

Progressive Systemic Sclerosis (Scleroderma)

CREST (calcinosis, raynaud’s, esophageal dysmotility, sclerodactyly, telangiectasias)

restrictive

 

Complications of Mechanical Ventilation

Barotrauma

Occurs when overdistended alveoli rupture.  Alveoli overdistension usually from selective ventilation of normal lung over diseased lung or from progressive air trapping.

Air can dissect along perivascular sheathes to cause pneumomediastinum, pneumothorax, and/or subcutaneous emphysema.

earliest radiographic sign is Pulmonary Interstitial Emphysema (PIE) demonstrated by small parenchymal cysts, linear streaks of air radiating towards the hilius, perivascular haloes, intraseptal air collections, pneumatoceles, and large subpleural air collections.

Classic x-ray findings of pneumothorax are seen in upright patients with apicolateral air.

Most common location in ICU patients are actually anteromedial and subpulmonic

Anteromedial pneumothoraces will show a  linear air density next to the mediastinum or increased sharpness of the mediastinal border

Subpulmonic pneumos can be seen by hyperlucency of upper abd quadrants and visualization of anterior costophrenic  sulcus.

Respiratory Complications of Critical Illness

Nosocomial Pneumonia and Ventilator-Associated Pneumonia

early pneumonia is present at the time of intubation or soon after.

late pneumonia is VAP

pathogenesis is colonization of the oropharynx followed by microaspiration.  Gram negative bacilli are capable of adhering to oropharyngeal cells; malnutrition, intubation,, illness, and ciliary dysfunction foster this adherence.  IgA and fibronectin breakdown also contribute to increased adherence during severe illness.  Pseudomonas can bypass the oropharynx and adhere directly to tracheal tissue due to its affinity for ciliated cells.

 

VAP is very difficult to diagnose as many entities, infectious and noninfectious, can cause fever.  Infiltrates can be from atelectasis, diffuse airway disease, PE, etc.  Antibiotics tailored to culture results may not even alter the outcome of true VAP (Parrillo).  Receiving antibiotics increases the chance of pseudomonas and acinetobacter infections and the mortality of these infections.

 

Protected brush specimens (PBS) avoid oropharyngeal or biofilm contamination.

 

Prevention

treat underlying disease, head elevated at 45°, nutritional support, assess if stress bleed prophylaxis is truly necessary, extubate as soon as possible,

Infection control procedures

Circuit changes every 48 hours on set-ups with humidifiers, remove tube condensate,

 

In the future, may see SDD, selective decon of the digestive tract using oral paste and swallowed antibiotics to eliminate colonization.  Current studies show decreased VAP but no change in mortality.

 

Capillary Leak Colloid still leaks out into the interstitium during sepsis and then it takes even more fluid with it. Blood does not leak even in sepsis Edema is bad, actually prevents nutrient delivery to cells Read book called Multi-System Organ Failure by Huddleston 2 of hydromorphone=10 morphine=.1 fentanyl ARDS-destruction of alveolar capillary network with pulmonary edema and hyaline membrane formation. Loss of compliance is due to loss of functional alveolar networks rather than inherent stiffness (at least at the beginning) So the lungs of an ARDS patient are not an adult patient’s, they are a baby’s. P-V curve (photocopy from the book) Can find the upper inflection point by switching to volume mode and raising amount of volume until a large increase in pressure is found PEEP improves gas exchange, redistributes lung water, reduces preload, and cardiac output It is end-inspiratory volume, not end-expiratory volume that causes lung injury Hypercapnia-decreases CO, increases HR, decreases afterload, Increased CBF, Decreased LOC, Cardiac effects are usually short-lived Hyperventilation takes ~3 minutes to equilibrate but hypoventilation takes ~15 minutes b/c CO2 must rebuild up Aa gradient should be <10 on Room Air, <100 on FiO2 1.0 As FiO2 goes up, there is increased V/Q mismatching Can test on 100% fiO2, if there is still an Aa gradient, then it is purely shunt Divide Aa by 20 on 100% to get shunt percentage P/F Ratio Physiologic Deadspace=Anatomic + Alveolar V ds / V T=PaCO2-PECO2/PaCO2 Normal = .35 to .15 Pressure to expand lung to a certain volume Plung=Palveolar-Ppleural C=delta V/delta Plung Decreased lung compliance in ARDS takes 1-2 weeks to develop The more you inflate the chest, the more it wants to recoil. If compliance changes during ventilation, then it is a sign of derecruitment (Pflex) (As alveoli are recruited, compliance improves) Choose fixed Vt then change PEEP

PEEP Equal to Pflex may be higher than needed once the lung begins to recruit

 

Pplat=end inspiratory pause pressure

 

Compliant lung is easy to distend

 

Abd distension causes poor (low) compliance

 

P End Exp=PEEP + Auto PEEP

 

AutoPEEP of lung as whole=Pressure c exp port occluded at end of expiratory

Measure just before next inspiration. Must wait at least 0.5 sec

End insp plat press at constant Vt is better

 

As you go supine, VC falls <20, With bilat diaphragmatic dysfunction, it falls >30

 

Insp collapse of IVC=hypovolemia

 

R vent infarction=Pra>Ppw

Tamponade=Pra=Ppw

 

Do not insert swans in LBBB

 

Caths are heparin-coated

 

Do rapid flush test before insertion to make sure system is not overdamped

 

if you do not get into PA on first attempt, turn clockwise

 

Consider turning off APRV or extending t-times so no fluctuations

A=atrial contraction–first wave to follow p

V=ventricular–at t wave

 

Air is compressible, so it leads to overdamping

 

If Pra does not fall with inspiration, then further volume will not augment CO

 

Pulmonary vasculature has enormous capacitance reserve

 

Reduced lung compliance blunts the effects of PEEP on Ppw

 

SVO2 should be measured by cooximetry  and not by calculations as at that point of ox disassoc curve large potential for error

 

copy 15-1,15-2,15-7

 

cuff pressure <25 mm/Hg

 

Vasodilators can eliminate hypoxemic vasoconstriction and therefore drop saturation

 

if mixed venous drops, then arterial sat will drop (especially if large amount of shunt)

 

Zone I can be created if pulmonary vascular pressure is low. Suspect if O2sat gets worse with PEEP

 

RQ Carbs=1

RQ Fat 0.7

RQ Lipogenesis=8.8

 

go back to nutrition chap 18

 

Circulatory Pathophysiology

more blood is ejected in systole than can run-off to the periphery, so some of the pressure is stored to use during diastole

 

cardiogenic shock, dobutamine and nitroglycerin

 

Shock=hypoperfusion

High CO2 decreased pH in heart cells decreasing Ca effects Give Calcium

 

Met acidosis does not cross intracellularly

In low CO, arterial pH doesn’t reflect the tissue, venous reflects it more

 

volume load until a drop in O2 sat

pancreatitis and cirrhosis look identical to sepsis (sterile endotoxemia)

 

ETCO2 to monitor PEEP, if it drops, either due to decreased CO or Zone 3 to Zone 1 transition. Either way, give volume

 

Bicarb and ionized Ca ma increase glycolysis

 

Clamp any ct with air leak to make sure it is not a drainage system issue

 

saline agitated injection to confirm placement on echo

 

PE creation of deadspace

Decreased CO may also lead to hypoxemia

Pulm HTN may also cause shunt through patent FO

Right heart ischemia rather than hypoxia is usually the killer in massive PE

 

Dobutamine is probably the best choice for BP augmentation

Return to 28 and 29

 

Respiratory

O2 Transport Hb, CO, O2 sat

can only load a small amount into the blood, loading Hb is much more important

Can decrease VO2 c intubation by off-loading respiratory muscles

Decrease fever for the same reason

table 30-3

decreased Co2=decreased Va

High Co2 c normal Vt=increased production or Increased VD/VT

 

Shunt=pneumonia, pulm edema, atelectasis

 

Type I

minimal Vt Shunt

Type II

deadspace

Type III

perioperative

decreased frc from atelectasis

Can we use lateral recumbent instead of proning

 

Type IV

Hypoperfusion

decreased mixed venous O2 from decreased cardiac output

especially prevalent if there is any shunt as venous blood goes directly to arterial

 

changing a volume mode to a decel flow pattern decreases pressures and increases flow to a broader area. majority of flow occurs at beginning of cycle when elastance is minimal and gives time for equilibration on damaged areas of lung. But in volume mode, this will also increase the inspiratory time and so the therefore decreased expiratory time may cause autopeep

 

ARDS=small lung not stiff lung initially

 

Type I

diffuse

fig 33-3, tab 33-1

fx of hypoxic pulmonary vasoconstriction

? of leukocyte and bacterial O2 utilization

pneumonia causes shunt, but adjacent areas have V/q mismatching

 

loss of drive

impaired neuromuscular competence

excessive respiratory load

 

problems in copd

decreased msucluar competence

PEEPi

 

fig 34-3

 

if you give 100% oxygen and CO2 rises, more likely secondary to worsening of V/Q mismatch

 

post-intubation

alkalosis-blow off too much CO2

hypotension-from PEEPi

 

resp muscles need 48-72 hours of rest; patient will sleep without sedation

 

COPDers are often malnourished

 

Load is resistive and elastic

 

Restrictive

Thoracic Deformity

High Vt or PEEP causes blood flow restriction and v/q mismatching

 

chap 37

 

BAL

>104 bacteria/cc as cutoff

 

liberation from mechanical ventilation

39-1 tab 39-2

lasix is key

 

Nif>25

P 0.1 <4 good, >6 bad

VC <10 cc/kg=failure

 

rapid/shallow <105 on t-piece rate/Vt

 

post extubation pulmonary edema from large negative pressure increasing left ventricular afterload

 

Review of Atelectasis

 

 

Dyspnea

Hemoptysis-TB, bronchiectasis, abcess, Wegener’s, Goodpasture’s, carcinoma, bronchitis

Nocturnal dyspnea can also be gerd

Platypnea-better when laying down, usually from shunt

Trepopnea-dyspnea in only one lateral position

Rhonchi, egophony, dull to percussion=consolidation

Hyperventilation

one study showed no correlation with CO2 levels.  CO2 was reintroduced to keep levels at normal and sx remained the same.  (Lancet 348(9021):154 July 20, 1996)

 

During attack PCO2 actually at baseline (Am J Psych 153(4):513 April, 1996)

 

Can cause St/T changes on EKG

 

 

 

 

 

 

 

 

 

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