{"id":5097,"date":"2011-07-14T20:23:23","date_gmt":"2011-07-14T20:23:23","guid":{"rendered":"http:\/\/crashtext.org\/misc\/respiratory-failure.htm\/"},"modified":"2013-11-23T19:13:31","modified_gmt":"2013-11-24T00:13:31","slug":"respiratory-failure","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/pulmonology\/respiratory-failure.htm\/","title":{"rendered":"Respiratory Failure"},"content":{"rendered":"<h2><span class=\"ez-toc-section\" id=\"Atelectasis\"><\/span>Atelectasis<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>not a causal factor in post-operative fever (Chest 2011;140(2):418)<\/p>\n<p>&nbsp;<\/p>\n<p>Respiratory Failure<\/p>\n<p>Type I-hypoxemic, PaO2&lt;60<\/p>\n<p>Type II-hypercapneic w\/wo hypoxemia, PaCO2&gt;50<\/p>\n<p>&nbsp;<\/p>\n<p>Mechanisms of Hypoxemia<\/p>\n<ol>\n<li>Inadequate PAO2\n<ul>\n<li>Alveolar Hypoventilation<\/li>\n<li>Decreased FiO2<\/li>\n<\/ul>\n<\/li>\n<li>V\/Q Mismatch<\/li>\n<li>Shunt (Will not improve with O2)\n<ul>\n<li>Intrapulmonary (Pneumonia, ARDS)<\/li>\n<li>Intracardiac<\/li>\n<\/ul>\n<\/li>\n<li>Diffusion Abnormality<\/li>\n<li>Low SvO2<\/li>\n<\/ol>\n<p>PAO2=FiO2(PB-PH2O) &#8211; PaCO2\/R<\/p>\n<p>R=.8<\/p>\n<p>&nbsp;<\/p>\n<p>Hypercapnea<\/p>\n<p>VT=VA+VD (Alveolar\/Deadspace)<\/p>\n<p>PaCO2=PACO2 in normal lungs<\/p>\n<p>&nbsp;<\/p>\n<p>Increased CO2 production (hypermetabolic states)<\/p>\n<p>Decreased Alveolar ventilation\/Increased deadspace ventilation<\/p>\n<p>Decreased Tidal Volume<\/p>\n<p>&nbsp;<\/p>\n<p>Reabsorbtion atelectasis and loss of hypoxic pulmonary vasoconstriction may actually cause hypoxemia to get worse in the presence of high fiO2 and shunt.<\/p>\n<p>&nbsp;<\/p>\n<p>article on the mechanisms of hypoxemia (intensive care medicine 2005;31:1017-1019)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Decreased PaO2 can actually lower respiratory drive in the critically ill, studies done in patients with cardiogenic shock.<\/p>\n<p>Primary neurologic problems can result in decreased respiratory drive.\u00a0 these include AML, spinal cord injuries, guillain-barre, and muscular disorders.<\/p>\n<p>Respiratory muscle fatigue from COPD\/Asthma, ARDS, etc.<\/p>\n<p>&nbsp;<\/p>\n<p>Increased production in sepsis, hypothermia, salicilates,<\/p>\n<p>Increased deadspace ventilation<\/p>\n<p>Hypercapnia can decrease respiratory drive.<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Non-pulmonary_Causes_of_Respiratory_Failure\"><\/span>Non-pulmonary Causes of Respiratory Failure<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Obesity-hypoventilation Syndrome-&#8220;Pickwickian&#8221;, obesity, sleep apnea, respiratory muscle weakness<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Immunologic_Lung_Disease\"><\/span>Immunologic Lung Disease<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<h3><span class=\"ez-toc-section\" id=\"Goodpastures\"><\/span>Goodpasture&#8217;s<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Antibasement membrane<\/p>\n<p>give immunosuppression and steroids<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Wegeners\"><\/span>Wegener&#8217;s<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Upper airway involvement<\/p>\n<h3><span class=\"ez-toc-section\" id=\"SLE\"><\/span>SLE<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>pneumonitis gets high dose steroids and cyclophosphamide<\/p>\n<p>Rheumatoid Arthritis<\/p>\n<p>interstitial fibrosis or BOOP<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Bronchiolitis_Obliterans_with_Organizing_Pneumonia_BOOP\"><\/span>Bronchiolitis Obliterans with Organizing Pneumonia (BOOP)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>acute illness with respiratory failure<\/p>\n<p>cough, dyspnea, flu-like syndrome<\/p>\n<p>restrictive lung pathology<\/p>\n<p>prednisone 1 mg\/kg\/day<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Idiopathic_Pulmonary_Fibrosis\"><\/span>Idiopathic Pulmonary Fibrosis<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>smokers are at the highest risk<\/p>\n<p>interstitial pneumonitis<\/p>\n<p>restrictive pathophysiology<\/p>\n<p>use low volumes and high rates<\/p>\n<p>increased risk of lung cancer and cardiac ischemia<\/p>\n<p>Progressive Systemic Sclerosis (Scleroderma)<\/p>\n<p>CREST (calcinosis, raynaud&#8217;s, esophageal dysmotility, sclerodactyly, telangiectasias)<\/p>\n<p>restrictive<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Complications_of_Mechanical_Ventilation\"><\/span>Complications of Mechanical Ventilation<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<h3><span class=\"ez-toc-section\" id=\"Barotrauma\"><\/span>Barotrauma<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Occurs when overdistended alveoli rupture.\u00a0 Alveoli overdistension usually from selective ventilation of normal lung over diseased lung or from progressive air trapping.<\/p>\n<p>Air can dissect along perivascular sheathes to cause pneumomediastinum, pneumothorax, and\/or subcutaneous emphysema.<\/p>\n<p>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.<\/p>\n<p>Classic x-ray findings of pneumothorax are seen in upright patients with apicolateral air.<\/p>\n<p>Most common location in ICU patients are actually anteromedial and subpulmonic<\/p>\n<p>Anteromedial pneumothoraces will show a\u00a0 linear air density next to the mediastinum or increased sharpness of the mediastinal border<\/p>\n<p>Subpulmonic pneumos can be seen by hyperlucency of upper abd quadrants and visualization of anterior costophrenic\u00a0 sulcus.<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Respiratory_Complications_of_Critical_Illness\"><\/span>Respiratory Complications of Critical Illness<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Nosocomial Pneumonia and Ventilator-Associated Pneumonia<\/p>\n<p>early pneumonia is present at the time of intubation or soon after.<\/p>\n<p>late pneumonia is VAP<\/p>\n<p>pathogenesis is colonization of the oropharynx followed by microaspiration.\u00a0 Gram negative bacilli are capable of adhering to oropharyngeal cells; malnutrition, intubation,, illness, and ciliary dysfunction foster this adherence.\u00a0 IgA and fibronectin breakdown also contribute to increased adherence during severe illness.\u00a0 Pseudomonas can bypass the oropharynx and adhere directly to tracheal tissue due to its affinity for ciliated cells.<\/p>\n<p>&nbsp;<\/p>\n<p>VAP is very difficult to diagnose as many entities, infectious and noninfectious, can cause fever.\u00a0 Infiltrates can be from atelectasis, diffuse airway disease, PE, etc.\u00a0 Antibiotics tailored to culture results may not even alter the outcome of true VAP (Parrillo).\u00a0 Receiving antibiotics increases the chance of pseudomonas and acinetobacter infections and the mortality of these infections.<\/p>\n<p>&nbsp;<\/p>\n<p>Protected brush specimens (PBS) avoid oropharyngeal or biofilm contamination.<\/p>\n<p>&nbsp;<\/p>\n<p>Prevention<\/p>\n<p>treat underlying disease, head elevated at 45\u00b0, nutritional support, assess if stress bleed prophylaxis is truly necessary, extubate as soon as possible,<\/p>\n<p>Infection control procedures<\/p>\n<p>Circuit changes every 48 hours on set-ups with humidifiers, remove tube condensate,<\/p>\n<p>&nbsp;<\/p>\n<p>In the future, may see SDD, selective decon of the digestive tract using oral paste and swallowed antibiotics to eliminate colonization.\u00a0 Current studies show decreased VAP but no change in mortality.<\/p>\n<p>&nbsp;<\/p>\n<p>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\u0092s, they are a baby\u0092s. 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 &lt;10 on Room Air, &lt;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<\/p>\n<p>PEEP Equal to Pflex may be higher than needed once the lung begins to recruit<\/p>\n<p>&nbsp;<\/p>\n<p>Pplat=end inspiratory pause pressure<\/p>\n<p>&nbsp;<\/p>\n<p>Compliant lung is easy to distend<\/p>\n<p>&nbsp;<\/p>\n<p>Abd distension causes poor (low) compliance<\/p>\n<p>&nbsp;<\/p>\n<p>P End Exp=PEEP + Auto PEEP<\/p>\n<p>&nbsp;<\/p>\n<p>AutoPEEP of lung as whole=Pressure c exp port occluded at end of expiratory<\/p>\n<p>Measure just before next inspiration. Must wait at least 0.5 sec<\/p>\n<p>End insp plat press at constant Vt is better<\/p>\n<p>&nbsp;<\/p>\n<p>As you go supine, VC falls &lt;20, With bilat diaphragmatic dysfunction, it falls &gt;30<\/p>\n<p>&nbsp;<\/p>\n<p>Insp collapse of IVC=hypovolemia<\/p>\n<p>&nbsp;<\/p>\n<p>R vent infarction=Pra&gt;Ppw<\/p>\n<p>Tamponade=Pra=Ppw<\/p>\n<p>&nbsp;<\/p>\n<p>Do not insert swans in LBBB<\/p>\n<p>&nbsp;<\/p>\n<p>Caths are heparin-coated<\/p>\n<p>&nbsp;<\/p>\n<p>Do rapid flush test before insertion to make sure system is not overdamped<\/p>\n<p>&nbsp;<\/p>\n<p>if you do not get into PA on first attempt, turn clockwise<\/p>\n<p>&nbsp;<\/p>\n<p>Consider turning off APRV or extending t-times so no fluctuations<\/p>\n<p>A=atrial contraction&#8211;first wave to follow p<\/p>\n<p>V=ventricular&#8211;at t wave<\/p>\n<p>&nbsp;<\/p>\n<p>Air is compressible, so it leads to overdamping<\/p>\n<p>&nbsp;<\/p>\n<p>If Pra does not fall with inspiration, then further volume will not augment CO<\/p>\n<p>&nbsp;<\/p>\n<p>Pulmonary vasculature has enormous capacitance reserve<\/p>\n<p>&nbsp;<\/p>\n<p>Reduced lung compliance blunts the effects of PEEP on Ppw<\/p>\n<p>&nbsp;<\/p>\n<p>SVO2 should be measured by cooximetry\u00a0 and not by calculations as at that point of ox disassoc curve large potential for error<\/p>\n<p>&nbsp;<\/p>\n<p>copy 15-1,15-2,15-7<\/p>\n<p>&nbsp;<\/p>\n<p>cuff pressure &lt;25 mm\/Hg<\/p>\n<p>&nbsp;<\/p>\n<p>Vasodilators can eliminate hypoxemic vasoconstriction and therefore drop saturation<\/p>\n<p>&nbsp;<\/p>\n<p>if mixed venous drops, then arterial sat will drop (especially if large amount of shunt)<\/p>\n<p>&nbsp;<\/p>\n<p>Zone I can be created if pulmonary vascular pressure is low. Suspect if O2sat gets worse with PEEP<\/p>\n<p>&nbsp;<\/p>\n<p>RQ Carbs=1<\/p>\n<p>RQ Fat 0.7<\/p>\n<p>RQ Lipogenesis=8.8<\/p>\n<p>&nbsp;<\/p>\n<p>go back to nutrition chap 18<\/p>\n<p>&nbsp;<\/p>\n<p>Circulatory Pathophysiology<\/p>\n<p>more blood is ejected in systole than can run-off to the periphery, so some of the pressure is stored to use during diastole<\/p>\n<p>&nbsp;<\/p>\n<p>cardiogenic shock, dobutamine and nitroglycerin<\/p>\n<p>&nbsp;<\/p>\n<p>Shock=hypoperfusion<\/p>\n<p>High CO2 decreased pH in heart cells decreasing Ca effects Give Calcium<\/p>\n<p>&nbsp;<\/p>\n<p>Met acidosis does not cross intracellularly<\/p>\n<p>In low CO, arterial pH doesn&#8217;t reflect the tissue, venous reflects it more<\/p>\n<p>&nbsp;<\/p>\n<p>volume load until a drop in O2 sat<\/p>\n<p>pancreatitis and cirrhosis look identical to sepsis (sterile endotoxemia)<\/p>\n<p>&nbsp;<\/p>\n<p>ETCO2 to monitor PEEP, if it drops, either due to decreased CO or Zone 3 to Zone 1 transition. Either way, give volume<\/p>\n<p>&nbsp;<\/p>\n<p>Bicarb and ionized Ca ma increase glycolysis<\/p>\n<p>&nbsp;<\/p>\n<p>Clamp any ct with air leak to make sure it is not a drainage system issue<\/p>\n<p>&nbsp;<\/p>\n<p>saline agitated injection to confirm placement on echo<\/p>\n<p>&nbsp;<\/p>\n<p>PE creation of deadspace<\/p>\n<p>Decreased CO may also lead to hypoxemia<\/p>\n<p>Pulm HTN may also cause shunt through patent FO<\/p>\n<p>Right heart ischemia rather than hypoxia is usually the killer in massive PE<\/p>\n<p>&nbsp;<\/p>\n<p>Dobutamine is probably the best choice for BP augmentation<\/p>\n<p>Return to 28 and 29<\/p>\n<p>&nbsp;<\/p>\n<p>Respiratory<\/p>\n<p>O2 Transport Hb, CO, O2 sat<\/p>\n<p>can only load a small amount into the blood, loading Hb is much more important<\/p>\n<p>Can decrease VO2 c intubation by off-loading respiratory muscles<\/p>\n<p>Decrease fever for the same reason<\/p>\n<p>table 30-3<\/p>\n<p>decreased Co2=decreased Va<\/p>\n<p>High Co2 c normal Vt=increased production or Increased VD\/VT<\/p>\n<p>&nbsp;<\/p>\n<p>Shunt=pneumonia, pulm edema, atelectasis<\/p>\n<p>&nbsp;<\/p>\n<p>Type I<\/p>\n<p>minimal Vt Shunt<\/p>\n<p>Type II<\/p>\n<p>deadspace<\/p>\n<p>Type III<\/p>\n<p>perioperative<\/p>\n<p>decreased frc from atelectasis<\/p>\n<p>Can we use lateral recumbent instead of proning<\/p>\n<p>&nbsp;<\/p>\n<p>Type IV<\/p>\n<p>Hypoperfusion<\/p>\n<p>decreased mixed venous O2 from decreased cardiac output<\/p>\n<p>especially prevalent if there is any shunt as venous blood goes directly to arterial<\/p>\n<p>&nbsp;<\/p>\n<p>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<\/p>\n<p>&nbsp;<\/p>\n<p>ARDS=small lung not stiff lung initially<\/p>\n<p>&nbsp;<\/p>\n<p>Type I<\/p>\n<p>diffuse<\/p>\n<p>fig 33-3, tab 33-1<\/p>\n<p>fx of hypoxic pulmonary vasoconstriction<\/p>\n<p>? of leukocyte and bacterial O2 utilization<\/p>\n<p>pneumonia causes shunt, but adjacent areas have V\/q mismatching<\/p>\n<p>&nbsp;<\/p>\n<p>loss of drive<\/p>\n<p>impaired neuromuscular competence<\/p>\n<p>excessive respiratory load<\/p>\n<p>&nbsp;<\/p>\n<p>problems in copd<\/p>\n<p>decreased msucluar competence<\/p>\n<p>PEEPi<\/p>\n<p>&nbsp;<\/p>\n<p>fig 34-3<\/p>\n<p>&nbsp;<\/p>\n<p>if you give 100% oxygen and CO2 rises, more likely secondary to worsening of V\/Q mismatch<\/p>\n<p>&nbsp;<\/p>\n<p>post-intubation<\/p>\n<p>alkalosis-blow off too much CO2<\/p>\n<p>hypotension-from PEEPi<\/p>\n<p>&nbsp;<\/p>\n<p>resp muscles need 48-72 hours of rest; patient will sleep without sedation<\/p>\n<p>&nbsp;<\/p>\n<p>COPDers are often malnourished<\/p>\n<p>&nbsp;<\/p>\n<p>Load is resistive and elastic<\/p>\n<p>&nbsp;<\/p>\n<p>Restrictive<\/p>\n<p>Thoracic Deformity<\/p>\n<p>High Vt or PEEP causes blood flow restriction and v\/q mismatching<\/p>\n<p>&nbsp;<\/p>\n<p>chap 37<\/p>\n<p>&nbsp;<\/p>\n<p>BAL<\/p>\n<p>&gt;104 bacteria\/cc as cutoff<\/p>\n<p>&nbsp;<\/p>\n<p>liberation from mechanical ventilation<\/p>\n<p>39-1 tab 39-2<\/p>\n<p>lasix is key<\/p>\n<p>&nbsp;<\/p>\n<p>Nif&gt;25<\/p>\n<p>P 0.1 &lt;4 good, &gt;6 bad<\/p>\n<p>VC &lt;10 cc\/kg=failure<\/p>\n<p>&nbsp;<\/p>\n<p>rapid\/shallow &lt;105 on t-piece rate\/Vt<\/p>\n<p>&nbsp;<\/p>\n<p>post extubation pulmonary edema from large negative pressure increasing left ventricular afterload<\/p>\n<p>&nbsp;<\/p>\n<p><a href=\"\/wp-content\/pdf\/atelectasis.pdf\">Review of Atelectasis<\/a><\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Dyspnea<\/p>\n<p>Hemoptysis-TB, bronchiectasis, abcess, Wegener&#8217;s, Goodpasture&#8217;s, carcinoma, bronchitis<\/p>\n<p>Nocturnal dyspnea can also be gerd<\/p>\n<p>Platypnea-better when laying down, usually from shunt<\/p>\n<p>Trepopnea-dyspnea in only one lateral position<\/p>\n<p>Rhonchi, egophony, dull to percussion=consolidation<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Hyperventilation\"><\/span>Hyperventilation<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>one study showed no correlation with CO2 levels.\u00a0 CO2 was reintroduced to keep levels at normal and sx remained the same.\u00a0 (Lancet 348(9021):154 July 20, 1996)<\/p>\n<p>&nbsp;<\/p>\n<p>During attack PCO2 actually at baseline (Am J Psych 153(4):513 April, 1996)<\/p>\n<p>&nbsp;<\/p>\n<p>Can cause St\/T changes on EKG<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[32],"tags":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v22.5 - 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