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
- Inadequate PAO2
- Alveolar Hypoventilation
- Decreased FiO2
- V/Q Mismatch
- Shunt (Will not improve with O2)
- Intrapulmonary (Pneumonia, ARDS)
- Intracardiac
- Diffusion Abnormality
- 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 patients, they are a babys. 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
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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