pulmo emergency
TRANSCRIPT
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Pulmo-emergency Panvilai
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50
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GASS.aureaus
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50
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Hypoxemia
DO2 = 1.38 x Hb x Osat + Pao2x0.003
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A-a gradient
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Hypoxemia : acute decompensation PaO2 < 60 mmHg activate peripheral
chemoreceptor
Minute vent.
Pul.art.vasoconstriction Right heart failure
sympathetic CO
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Diffusion of gas CO2 > O2 > CO > NO Gas pulmonary
edema Pulmonary capillary RBC rbc
cell
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Normal A-a gradient Hypovantilation Low FiO2 ( high attitude)
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Wide A-a gradient
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Right to left shunt Clinical : hypoxemia despite oxygen supplement, wide Aa gradient Pathology :pulmonary consolidation, pulmonary atelectasis,
and vascular malformations.
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V-q mismatch Clinical : increased A-a O 2 gradient and
hypoxemia improves with supplemental oxygen. PathologyPulmonary emboli, pneumonia, asthma, COPD,
and extrinsic vascular compression
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Respiratory center central hypercapnic chemoreceptors in the
central medulla. peripheral hypoxic chemoreceptors, primarily in
the carotid body in concert with those in theaortic arch.
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Respiratory physiology Minute ventilation= TV (7 ml/kg)* f (respiratory rate)Min.vent maintain PaCO 2 = 4oIncrease CO 2 production increase MVDecrease CO2 production decrease MV
MV < 2 L /min respiratory acidosis
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Minute ventilation
Minute VentilationVE = VT x f New PaCO2x VE = Old PaCO2x VE
Case ICP set ventilator VT = 500 ml , f =12
PaCO2 = 50 mmHg if want PaCO2 = 40 mmHgsetting VT
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New PaCO2x VE = Old PaCO2x VE
40 x 500 x f = 50 x 500 x 12 f = 15
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Dead space = Volume air Physiologic dead space (30 % TV)=
1. Anatomical dead space =trachea, bronchi, and bronchioles
2.Alveolar dead space = absent of alveolar
capillary perfusion with normal ventilation (high v/q mismatch)Disease: COPD,ARDS
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Expired air In patients with normal lungs, ETCO 2 is
approximately 3 mm Hg lower than PACO 2,
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Cyanosis Deoxy Hb > 5 g/dl Met Hb: 1.5 g/dl SulfHb: 0.5 g/dl
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Pseudocyanosis Clinical : not branch with pressure heavy metals [e.g., iron (hemochromatosis),
gold, silver, lead, and arsenic] drugs (e.g., phenothiazine, minocycline,
amiodarone, and chloroquine)
Chrysiasis: rare complication of gold treatment Argyria; chronic ingestion /application of silver
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Arterial blood gas interpretation
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Normal ABG value pH = 7.35 7.45 ( 7.4 +-0.5 ) PaO2 = 80 100 mmHg PaO2 < 80 mmHg = Mild hypoxemia PaO2 < 60 mmHg = Moderate hypoxemia PaO2 < 40 mmHg = Severe hypoxemia
New born = 40 60 mmHg Age > 60 PaO2 = 100 [0.25 x Age (Yr)]
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ABG error Excessive heparin affectspH, PCO 2, and PO 2 Air bubbleslowering the PCO 2 values with an increase in pH
and PO 2.
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PaCO2 = 35 45 mmHg (40 +-5 mmHg) HCO3 = 22 26 mEq/L (24 +-2 ) BE = +-2.5 SaO2 = 95 100 %
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Table 26-2 Expected Pa O2 in Patients Inhaling Various
Concentrations of Oxygen, mm Hg
FIO 2 0.21 (room air) 0.4 0.6 0.8 1.0
PaO 2* 100 227 370 512 655
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Aa-gradient
measures how well alveolar oxygen istransferred from the lungs to the circulation
A normal P(A-a) O 2 is under 10 mm Hg in young, healthy patients predicted by the formula P(A-a)O 2 = 2.5 + 0.21
(age in years) ( 11).
P(A-a)O 2 = 145 PaCO 2 PaO 2.
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ABG interpretation
PaCO2 =hypoventilation PaCO2 =hyperventilation
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gas
Alveolar air equation
PAO2 = 713xFiO2-1.2xPaCO2 (FiO2 < 0.6) PAO2 = 713xFiO2-PaCO2 (FiO2 > 0.6)
(A-a)DO2 = PAO2 PaO2
(A-a)DO2 = 140 (PaO2 + PaCO2)
Normal (10-20mmHg)
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PaO2/FiO2 < 400 < 400 lung injury < 200 ARDS
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Acid-base pH predicted pH and measured pH Delta pH = Delta PaCO2 x (1/100) Delta pH = Delta PaCO2 x (1/200) predicted pH < measured pH = acidosis
predicted pH > measured pH = alkalosis
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PaCO2 PaCO2 If PaCO2 pH =Ventilatory Cause
PaCO2 increase =respiratory acidosis
PaCO2 decrease =respiratory alkalosis
If PaCO2 pH =Ventilatory compensation
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Respiratory acidosis
Acute PaCO2 10 mmHg HCO3 1 mEq/L
Chronic PaCO2 10 mmHg HCO3 4 mEq/L
Acute: HCO3 = 0.1 PaCO2 Chronic: HCO3 = 0.4 PaCO2
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Respiratory Alkalosis
Acute PaCO2 10 mmHg HCO3 2 mEq/L
Chronic PaCO2 10 mmHg HCO3 5-6 mEq/L
Acute: HCO 3 = 0.2 PaCO 2Chronic: HCO 3 = 0.5 PaCO 2
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HCO3 HCO3 pH = metabolic cause HCO3 =metabolic acidosis
HCO3=metabolic alkalosis
PaCO2 and HCO3
Met acido PaCO 2 = (1.5 x HCO 3)+8+/-2 mmHg Met alkalo PaCO 2 = (0.7 x HCO 3)+20 mmHg
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Anion gapNa (HCO3 + Cl)
NaHCO30.2xBWxBE mEq
0.2xBWx(24-HCO3) mEq
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Metabolic acidosis HCO 3 < 22Predicted PaCO 2 = 1.5(HCO 3)+82
AG = Na (Cl+ HCO 3) -12 High AG - salicylate, methanol
- -azotemic renal failure -DKA -uremia -lactic
acid
-carbonic anhydrase inhibitor -ion exchange resin
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normal AG HCO 3
-GI-diarrhea -small bowel fistula -ileostomy -ureterostomy colostomy
-kidney -RTA Cl
-Hydrochloric acid -NaCl -ammonium chloride
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AG / HCO3
< 0.8 mixed high gap, normal gap0.8-1.2 pure high gap metabolic acidosis> 1.2 - mixed high gap ,metabolic
alkalosis
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= (Na + + K +) Cl- = Unmeasured anion - Unmeasured cation + Increased AG
Increased UA - high AG metabolic acidosis,hyperalbuminemia, metabolic alkalosis
Decreased AG Decreased UA - hypoalbuminemia
Increased UC - Li+, cationic IgG
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Metabolic alkalosis HCO 3 >26 mEg/l predicted PaCO2= 0.7 ( HCO3 ) +20
PaCO 2 55-60 mmHg
- - ,NG suction -
-NaHCO 3 -Ringer lactate /acetate - citrate
- K - - aldosterone - steriod - Insulin - CO2 (Eucapnic ventilation
posthypercapnia )
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hiccup
Vagal and phrenic nerve
cute: Benign, Self-limited
Chronic: Persistent, Intractable
Gastric distention Central nervous system structural lesions
lcohol intoxication Vagal or phrenic nerve irritation
Excessive smoking Metabolic: uremia, hyperglycemia
brupt change inenvironmentaltemperature
General anesthesia
Psychogenic Surgical procedures: thoracic, abdominal,prostate and urinary tract, craniotomy
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Hiccup Persistence during sleep suggests an organic cause,
and resolution during sleep suggests a psychogenic
cause Treatment1. the pharynx will block the vagal portion of the
reflex arc and abolish the hiccups2. Med:chlorpromazine 25-50 mg IV q 2-4 hr
Plasil 10 mg IVoral treatment can be initiated with nifedipine 10 to
20 mg tid or qid, valproic acid 15 mg/kg per dtaken tid, or baclofen 10 mg tid
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Pleural effusion Positive sign of pleural effusion in upright chest
filmFluid 150-200 ml In CHF: thoracentesis is reserved for those
patients who do not resolve in 3 to 4 days afterdiuresis
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Light criteria for pleural effusion Sensitivity 98 % Specificity 65-86 %Exudate criteria1. Pleural fluid/serum protein > 0.52. Pleural fluid /serum LDH > 0.6
3. Pleural fluid LDH > 2/3 upper limit LDH
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Pleural fluid Cytology : highest yield is with adenocarcinoma ,
much lower with squamous cell, lymphoma, ormesothelioma
Neutrophil: parapneumonic, PE,pancreatitis Amylase; pancreatitis, rupture esophagus
pH < 7.10 = empyema thoraces If diuretic use : serum to pleural albumindifference of greater than 1.2 g/dL = exudate
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Spontaneous pneumothorax Spontaneous absorption rate 1-2% per d 100% 02 increase rate 3-4x
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Diagnosis of pneumothorax "gold standard"the 6-foot upright PA chest radiographthe sensitivity = 83 percent
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Diagnosis of pneumothorax Ultrasonography : sensitivity 100 percent. Sonographic signs of a pneumothorax include (1) absence of lung sliding (2) "lung point" (3) absence of vertical comet-tail artifacts
arising from the pleural line on a B-mode two-dimensional view.
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DL = the diameter of the
lung measured at thehilar level
DHT is the internaldiameter of thehemithorax measuredat the hilar level.
DL
size of PTX ( in %) =( 1 DL3 / DHT 3 ) x
100
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Primaryspontaneous
Pneumothorax
Small(3 cm apex to cupola)
no increase in pneumothorax
Oxygen 3-4 lpm
repeat chest radiograph in12 to 48 h
ASPIRATE > 4 L
NO
OBSERVE 6 HR
NO RECURRENCED/C FU 24 hr
24 to 28 Frtube with
water seal(no suction).
6 hr
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Indication for ICD 1. secondary spontaneous pneumothorax,2. recurrent pneumothorax3. abnormal vital signs
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Risk of reexpansion pulmonary edema aged 20 to 39 years larger pneumothoraces present for >72 h rapidly expanded with suction.
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Iatrogenic pneumothorax Treatment for iatrogenic pneumothorax
parallels that for spontaneous pneumothorax Hospitalization if post subclavian or pleural biosy
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Treatment ATB no indication
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Pneumonia Pneumococcal lobar Atypical-hilar adenopathy Lung abscess- staph, klebsiella Lung mass-staph, pneumococcal Alcohol-increase oral GN pathogen-
pneumococcal and increaseklebsiella,Haemophilus spp. DM- pneumonia and mycolplasma
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Atypical pneumonia Legionella : GI symptom Chlamydia : associate with adult onset asthma
Mycoplasma :extrapulmonary symptoms1. bullous myringitis2. Rash3. neurologic symptoms4. arthritis and arthralgia5. hematologic abnormalities6. rarely, renal failure.
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Pneumonia in elderly High mortality Atypical legionella Postinfluenza bacterial pneumonia is most
commonly caused by S. pneumoniae, S. aureus, and H. Influenzae
Initially afebrile 1/3 no leukocytosis
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Pneumonia in elderly Poor prognostic indicators1. hypothermia or T > 38.3C (100.9F)2. a low white blood cell count3. Immunosuppression4. gram-negative or staphylococcal infection
5. cardiac disease6. bilateral infiltrates7. extrapulmonary disease
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Nursing home acquired pneumonia Streptococcus pneumoniae, gram-negative bacilli, and Haemophilus influenzae
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Pneumonia in transplant First 3 mo. : GNB (especially Pseudomonas
aeruginosa ), Staphylococcus aureus, and
Legionella predominate > 6 mo.= CAP pathogen
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Lung abscess Most = anaerobe Aerobe bacteria -- More common in
immunocompromise Rx; clinda + 2 nd ceph or ampi/sulbactam
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pathogen Community acquire Streptococcus pneumoniae, Staphylococcus
aureus, Haemophilus influenzae, and Enterobacteriaceae
hospital-acquired aspiration pneumonia Pseudomonas aeruginosa and gram-negative
organisms in Anaerobe: chronic alcoholism, putrid sputum,
lung abscess, periodontal disease
Syndrome and Clinical Antibiotic (Usual Dose)*
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Syndrome and ClinicalSituation
Antibiotic (Usual Dose)*
Aspirationpneumonitis
Signs or symptomslasting >48 h
Levofloxacin 500 mg per dorCeftriaxone 1 2 g per d
Small bowelobstruction or use ofantacids orantisecretory agents
Levofloxacin 500 mg per dorCeftriaxone 1 2 g per d,orCiprofloxacin 400 mg every 12 horPiperacillin tazobactam 3.375 g every 6 horCeftazidime 2 g every 8 h
Aspirationpneumonia
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Community-acquired
Levofloxacin or Ceftriaxone
Residence ina long-termcare facility
Levofloxacin 500 mg per dorPiperacillin tazobactam 3.375 g every 6 horCeftazidime 2 g every 8 h
Severeperiodontaldisease,putridsputum, oralcoholism
Piperacillin tazobactam 3.375 g every 6 hImipenem 0.5 1.0 g every 6 8 hLevofloxacin 500 mg per d plusclindamycin 600 mg every 8 hmetronidazole 500 mg every 8 hCiprofloxacin 400 mg every 12 h plusclindamycin 600 mg every 8 h ormetronidazole 500 mg every 8 hCeftriaxone 1 2 g per d plus clindamycin600 mg every 8 hmetronidazole 500 mg every 8 h
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Hemoptysis Mild < 20 mL of blood in 24 h moderate : 20 to 600 mL in 24 h
massive hemoptysis >600 mL in 24 h, > 200ml/time
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Etiology of hemoptysis Infectious: bronchitis, pneumonia, lung abscess, TB Neoplastic: lung cancer, bronchial adenoma Cardiovascular: PE, MS, CHF, pulmonary hypertension, pulmonary
angiodysplasia Alveolar hemorrhage syndromes: Behet syndrome, Goodpasture
syndrome, Wegener granulomatosus Hematologic: uremia, platelet dysfunction, anticoagulant therapy Traumatic: FB aspiration, ruptured bronchus, arterio-
tracheobronchial fistula (aortic aneurysm) Iatrogenic: bronchoscopy, lung biopsy Inflammatory: bronchiectasis, cystic fibrosis
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Common cause of massive hemoptysis
Bronchiectasis TB
CA Aneurysm Pulmonary angiodysplasia Lung abscess
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treatment
Position bleeding lung down ET tube No 8 to allow bronchoscope
coagulopathy : FFP Med; cough suppressant
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Lung transplant
Signs of rejection includecough, chest tightness, fever ( 0.5C above baseline),
hypoxemia, decline in FEV 1 ( 10 percent), and thedevelopment of infiltrates on the chest radiograph Ddx from infection by bronchoscopy Rx: methylprednisolone 500-1000 mg
Cytomegalovirus is the most commonly encountered viral agent implicated in posttransplant pulmonaryinfection
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Active TB
thin-walled cavities (5 mm) tend to be infective and, when thick-walled (10 mm), squamous cell
carcinoma of the lung enters into the differential diagnosis differential diagnoses of cavitarypulmonary lesions include infections from
Staphylococcus, Klebsiella, anaerobes,and non-infectious causes like squamous cell
carcinoma of the lung, pulmonaryinfarcts, Wegeners granulomatosis, and rheumatoid
nodules
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TB
Gold standard = C/s XDR = INF + Rifam
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Pulmonary embolism
Site of clotMost = lower ext.
RiskHereditary: antithrimbun/proteinc-s def, factor V
laden, antiphospholipid Acquire : malignancy, trauma, major surgery, post
partum in 1 month, pregnancy, polycythemia vera, reduced mortality, obese, central venouscatheter, bedrest > 48 hr
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Chest film in PE
Unilateral basilar atelectasis Western mark (oligemia)
Hamptonhump
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Pleural basedopacity
Lunginfarction
Hamptonshump
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Pulmonaryoligemia
WesternMark Sign
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tintinalli
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ECG
Symmetrical T inversion can present in lead V1- V4
Most = sinus tachycardia S13T3 is nonspecific
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echo
Differential with V-infarc good apex motion RV dilate (Normal RV diameter is not greater
than 2.5 cm)
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All of the following statements are TRUE about diagnostictests for PE EXCEPT
(A) The V /Q scan is 98 percent sensitive and 35percent specific for PE
(B) Duplex ultrasound is 95 percent sensitive and
95 percent specific for DVT(C) The difficulty in using V/Q scan findings forthe diagnosis of PE is the lack of a standardizeddefinition for clinical suspicion
(D) A D-dimer of less than 500 U/mL has a negativepredictive value of 90 percent
(E) Spiral CT is up to 90 percent sensitive and 96percent specific for PE
10%
D-dimer
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D dimer
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D-dimer
Best = elisa assay At 500 ng/dl (sense 94,spec 55)
False negative; on warfarinFalse positive 1 wk after surgery, pregnancy or
post partum, malignancy pretest propability < 40 %
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Diagnosis
Low to moderate prop in VQ CTA Normal VQ ruled out
High prop with negative CTA furtherinvestigation
Positive VQ in case of pretest propability < 40%-> further investigation
Positive VQ in case of pretest propability >40%=diagnosis
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PE: spiral CT versus VQ
Specificity of spiral CT= high probability VQSensitivity of spiral CT=low probability VQ
Spiral Use of contrast False negative insubsegmental PE Helpful in nondiagnostic VQ(COPD,PARENCHYMAL LUNGDIS.)
Negative VQmore sense
than negativespiral CT
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pregnancy
upper limit of a normal D-dimer increases witheach trimester of pregnancy but should not
exceed 1000 g/L at any time half-dose injection of radioactive material to
perform a perfusion lung scanOr a CT angiogram without indirect venography can be performed and the uterus shielded duringimage acquisition (< VQ)
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obese
> 190 kg Use doppler us and D-dimer to guide
You respond to a code blue on the labor -and-delivery ward. The nurse tells you that the patient is a previously healthy 41-year-old African-American
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y p p y y y woman, 4 days status post normal spontaneous vaginal delivery. Shecomplained of chest pain and dyspnea and then fell to the floorunconscious. No seizure activity was noted. Although initially pulseless, vital signs returned with assisted ventilations. You find the patientconfused, grunting, and cyanotic. Vital signs are BP 68/50 mm Hg, HR 121 beats per minute (sinus tachycardia), and RR 28, with pulse oximetry of 78percent on high-flow oxygen.
Physical examination shows distended neck veins, normal heart sounds with aprominent S2, a thready pulse with cool, cyanotic extremities, and adequatetidal volume with no rales or wheezes. Chest x-ray is normal. Bedsideultrasound of the heart shows a dilated right ventricle with parodoxicalseptal wall motion. In addition to immediate intubation and fluidresuscitation, what is the MOST appropriate therapeutic intervention?
(A) Emergent diagnostic spiral CT(B) Heparin bolus of 80 U/kg intravenously followed by 18 U/kg infusion(C) LMWH 1 U/kg every 12 h(D) r-tPA at a dose of 100 mg over 2 h(E) Emergent transfer to the angiography suite for pulmonary arteriography
and local infusion of urokinase
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Anticoagulant
IV UFH or SC LMWH for initial treatment ofPTE
With/without overlapping with warfarin Recommend LMWH SC over IV UFH in acutenonmassive PTE
LMWH SC/IV UFH for at least 5 days
In renal failure recommend IV UFH over LMWHSC
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anticoagulant
Prefer LMWH (grade Ia) if high risk for bleeding ,obese, renal insufficiency
monitor factor 10 A Massive PE heparin 80 U/kg bolus then 18
/kg/hr Enoxaparin 1 mg/kg sc bid
with a pretest probability >50 percent, empiricheparin should be administered
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Thrombolytic
Definite= PE with cardiogenic shock Other clinical judge case by case including
severe hypoxia Use sk- 250,000 u IV over 30 min then 100,000
/hr for 24 hr
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Surgery; RV emboli Severe refractory hypotension
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PE with arrest
CPR no pulse returns within a few minutes bolus inject 100 mg of alteplase or an equivalent
dose of fibrinolytic therapy whilecardiopulmonary resuscitation is continued forat least 20 min ROSC image to locateembolus surgical thrombectomy
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Pitfall
hypercoag state heparin(LMWH has no effect)
Ventilation/Perfusion scintigraphy Required cooperation Not proper for unstable cases
Pulmonary CTA Not available Required contrast agent
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Systemic/local thrombolysis Acute massive PTE with clinical unstable Systemic thrombolysis is recommend, unless
contraindicated Recommend not to use local thrombosis Short term thrombolysis over long term infusion In those case, CVT should be consulted as initial
management
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Thrombus defragmentation therapySurgical thromboembolectomy Only in unstable case with contraindicate for
thrombolysis
Until now no evidence of benefit over lytictherapy
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COPD with AE
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Acute asthmatic attack
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Asthma in Pregnancy
No side effect of medication (B2-agonists,sterods) but fetal hypoxia may be greater risk
Physiologic hyperventilation leads to higher PaO2;
if PaO2 less than 70 mmHg represents severehypoxemia
less than 35 mmHg represents respiratory failure
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Anterior mediastinal mass
Obscure heart border differential diagnoses of masses in the
anterior mediastinum include the 5 T s:thyroid masses, teratoma, thymic masses,
(terrible) lymphoma, and thoracic aneurysm.
53
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74 yo man with COPD WITH AE After start
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74 yo man with COPD WITH AE. After start
bipap with I 10 E 4 20 , rate 10, 20 min later thepatient oxygenation is not improve which of thefollowing change most likely increase patientoxygenation.
a) increase in IPAP for 10-15 b) Increase rate from 10-12c) Decrease EPAP from 4 to 2d) Increase EPAP from 4 to 7 IPAP from 10-15e) Decrease EPAP from 4 to 2 and IPAP from 10
to 5
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BIPAP
oxygenation.: PEEP (concomitantly increaseIPAP to maintain positive pressure
differentiation during inspiration) and Fio2 PaCO2: rr
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Non invasive1. Consciousness( CO2 retension 15-
30 )
2. Co-operate3. CVS stable4. Asphyxia, aspiration, airway obstruction ect5. PaO2 < 60 with 100%O2
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Problem with NPPV Oxygen concentration Rebreathing esp EPAP< 4 cmH2O
Dyssynchrony Rise time
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BiPAP IPAP ~8 cmH2O acute 10-16
20 ( OSA 40) EPAP;Rebreathing esp EPAP< 4 cmH2O Back up rate 12-24 Rise time 0.05-0.1 sec 0.3-0.4 sec Maximum inspiratory time I:E
1:1 Blender, Humidifier
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COPD pH > 7.30-7.35
PaCO2 45-60 mmHg RR >25 Accessory muscle,paradoxical abdominalmotion
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63 yo woman present with ARDS. Which of the
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63 yo woman present with ARDS. Which of thefollowing summarized best ventilationstrategies in ARDS?
a) Owing to low compliance, pt need higher TV,higher PEEP to ensure adewuate ventilaiton
b) Owing to significant airway obstruction, ptrequire very low or no PEEP similar to asthmato avoid air trapping
c) Owing to low compliance , pt require low TV,and higher PEEP to avoid barotrauma
d) Owing to high compliance, pt donot requirePEEP
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ALI and ARDS Bilateral pulmonary infiltration or edema without LV failure (PCWP
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0.4-0.60.210.4-0.61.00.4-0.6FiO 2
Deceleratingor square
Deceleratingor square
Deceleratingor square
DeceleratingDeceleratingwaveform
5-100-335-15 5PEEP
606060-10040-8040Peak flow
(L/min)
10-1410-148-1212-208-12RR
8-1212-148-106-810-12VT(ml/kg)
SIMVSIMVSIMV
Due to low TV, give higher PEEPto keep adequate oxygenation
(FiO2 < 0.5)
A/C,SIMV
A/C A/C,SIMV
A/C A/C orSIMV
Mode
EDCB Asettingcondition
CHFNeuromuscCOPDARDSPeriop
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0.4-0.60.210.4-0.61.00.4-0.6FiO 2
Deceleratingor square
Deceleratingor square
Deceleratingor square
DeceleratingDeceleratingwaveform
5-100-335-15 5PEEP
606060-10040-8040Peak flow
(L/min)
10-1410-148-1212-208-12RR
8-1212-148-106-810-12VT(ml/kg)
SIMVSIMVSIMV
GoalKeep pH normal
O2Sat >90%Pplat
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following objective
a) Pt purposefully hypoventilated, maintainingelevated PaCO2 to keep airway pressure at safelevel
b) Pt purposefully hyperventilated to bring PaCO2 back to normal because ventilatory failure isprimary reason for intubation
c) Initial ventilator setting are no different thanpatient intubated for altered mental status
d) Inspiratory flow rates are set very low to avoidcausing very high peak airway pressures
e) The inspiratory flow curve should be ramp-style wave instead of square style wave to maximizedexpiratory times
A/C,SIMV
A/C A/C,SIMV
A/C A/C orSIMV
Mode
EDCB Asettingcondition
CHFNeuromuscCOPDARDSPeriop
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0.4-0.60.210.4-0.61.00.4-0.6FiO 2
Deceleratingor square
Deceleratingor square
Deceleratingor square
DeceleratingDeceleratingwaveform
5-100-335-15 5PEEP
606060-10040-8040Peak flow
(L/min)
10-1410-148-1212-208-12RR
8-1212-148-106-810-12VT(ml/kg)
SIMVSIMVSIMV
A/C,SIMV
A/C A/C,SIMV
A/C A/C orSIMV
Mode
EDCB Asettingcondition
CHFNeuromuscCOPDARDSPeriop
DHII t i i PEEP
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0.4-0.60.210.4-0.61.00.4-0.6FiO 2
Deceleratingor square
Deceleratingor square
Deceleratingor square
DeceleratingDeceleratingwaveform
5-100-335-15 5PEEP
606060-10040-8040Peak flow
(L/min)
10-1410-148-1212-208-12RR
8-1212-148-106-810-12VT(ml/kg)
SIMVSIMVSIMVIntrinsicPEEP
autoPEEPDynamicairway collapse
Maximizeexp.time to
avoid air trap by shorten
inspitime(highinsp.flow) andsquare wave
form, decrease
min.vent ( Vt or RR)
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