respiratory Flashcards
chronic bronchitis defination
chronic productive cough for
atleast 3mnths
in 1 year
for 2 consecutive years
effect of excess oxygen in COPD
In advanced chronic obstructive pulmonary disease (COPD), destruction of the terminal bronchioles and alveoli causes areas of physiologic dead space to develop. The affected regions have limited surface area available for gas exchange, which leads to ventilation/perfusion (V/Q) mismatch causing local hypoxia and hypercapnia.
Hypoxia induces selective vasoconstriction in these areas of the lung and redirects blood flow to better ventilated alveoli, reducing V/Q mismatch.
Supplemental oxygen improves hypoxia but can cause C02 retention by the following mechanisms:
• Loss of compensatory vasoconstriction in areas of ineffective gas exchange worsens V/Q mismatch
• Increase in oxyhemoglobin reduces the uptake of C02 from the tissues by the Haldane effect
• Decreased respiratory drive and slowing of the respiratory rate causes reduced minute ventilation The acidosis caused by an acute increase in C02 increases brain gamma-amino butyric acid and glutamine and decreases brain glutamate and aspartate, causing a change in level of consciousness. Hypercapnia also causes reflex cerebral vasodilation and may induce seizures, as seen in this patient
. Oxygen should be used cautiously with a goal Sa02 of 90%-93% or Pa02 60-70 mm Hg. Patients who develop significant acidosis or have severely reduced level of consciousness require mechanical ventilation.
bohr effect
⬆️ pco2》⬆️H+》⬇️hb affinity for o2》⬆️o2 unloading
occurs at tissue level
haldane effect
⬆️pO2⬆️unloading of CO2 at alveoli level
Oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin which increases the removal of carbon dioxide. This property is the Haldane effect. Conversely, oxygenated blood has a reduced affinity for carbon dioxide.
cause of leukocytosis after treatment of aasthma exacerbation
patient being treated for an asthma exacerbation now has leukocytosis with
neutrophilic predominance, which is a common effect of systemic glucocorticoids (eg,
methylprednisolone).
Glucocorticoid use causes a leukocytosis due to the following:
• Mobilization of marginated neutrophils into the bloodstream (predominant
mechanism
): Marginated neutrophils are attached to the endothelium of blood
vessels: glucocorticoid-induced mobilization of these neutrophils leads to a higher
number of circulating neutrophils
• Stimulation of release of immature neutrophils from the bone marrow (as evidenced
by the 3% band forms in this patient)
• Inhibition of neutrophil apoptosis
In contrast, glucocorticoids decrease the number of circulating lymphocytes and
eosinophils through a combination of increased apoptosis, increased emigration into the
tissues, and decreased production
theophylline toxicity cause and symptoms
Theophylline has a
narrow therapeutic index, and toxicity can occur from accumulation by reduced clearance
or decreased metabolism due to saturation of metabolic pathways. Theophylline is
metabolized predominantly by the cytochrome oxidase system in the liver. Inhibition of
these enzymes by concurrent illness (eg, cirrhosis, cholestasis, respiratory infections with
fever) or drugs (eg, cimetidine, ciprofloxacin, erythromycin, clarithromycin, verapamil) can
raise serum concentration and cause toxicity.
Symptoms of toxicity usually manifest as central nervous system stimulation (eg,
headache, insomnia, seizures), gastrointestinal disturbances (eg, nausea, vomiting), and
cardiac toxicity (arrhythmia).
This patient recently began taking ciprofloxacin, a drug
known to decrease clearance of theophylline. Therefore, the best next step is to
measure serum theophylline levels to assess for toxicity.
uses of non invasuve positive pressure ventilation
Noninvasive positive-pressure ventilation (NPPV) is ventilatory support delivered by
facemask rather than endotracheal tube; it can be delivered in several different modes,
including continuous positive airway pressure and bilevel positive airway pressure.
NPPV decreases work of breathing, improves alveolar ventilation, and is the preferred
method of respiratory support in patients with AECOPD. Physiologic benefits include a
decrease in respiratory rate and arterial carbon dioxide tension (PaCOzl, with an increase
in tidal volume, minute ventilation, and arterial oxygen tension (PaOzl. NPPV in patients
with AECOPD is associated with a decrease in mortality, intubation rate, treatment
failure, length of hospital stay, and incidence of nosocomial infection.
if it fails then⬇️
Invasive mechanical ventilation may be required in hypercapnic patients with
poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions),
hemodynamic instability, or profound acidemia (pH <7.1 ). This patient’s pH of 7.32 and
PaC02 of 60 mm Hg suggest a mild to moderate acute respiratory acidosis on an existing
chronic respiratory acidosis. A trial of NPPV is warranted prior to intubation, especially
as advanced COPD may make weaning and extubation more challenging. If this patient
fails a 2-hour trial of NPPV (eg, h
A-a pressure gradient
PE causes ventilation/perfusion (V/Q) mismatch, resulting in an increase from the expected alveolar-arterial (A-a) oxygen gradient.
Alveolar oxygen (PAOzl is calculated as follows:
PA02 = (Fi02 x [Patm-PH,Q))-(PaC0/0.8)
where Fi02 = fraction of inspired oxygen, Patm = atmospheric pressure, PH20 = water vapor pressure, and PaC02 = partial arterial pressure of carbon dioxide (obtained from arterial blood gas [ABG) results).
This simplifies to PA02 = 150-(PaC0/0.8) for patients breathing room air at sea level.
The A-a gradient is then calculated by subtracting PA02-Pa02, where Pa02 = partial arterial pressure of oxygen (also from ABG results). The A-a gradient is elevated if it is higher than the expected A-a gradient on room air, estimated by (2.5 + [0.21 x patient age)) or (patient age/4 + 4).
A-a gradient elevation occurs in processes that cause impaired gas exchange.
tram track sign is seen in
Tram-track signmay be used in chest radiography or CT to denote the thickened non-tapering (parallel) walls ofcylindrical bronchiectasis.
string of beads in radiology
String of beads in radiology- Fibromuscular dysplasia Chr. Pancreatitis (chain of lakes) Small bowel obstruction varicose bronchiectasis
clinical features of sarcodosis
systemic granulomatous ds characterised by noncaseating granulomas
constitutional symptoms of fever anorexia wht loss
organs involved
lungs
cough dyspnea
skin
erythema nodosum
lupus pernio
eyes
ant and post uveitis
heart
arrythmias
heart block
musculoskeletal
arthritis arthralgia
nervous
cn paralysisdiagnosis of sarcodosis
CXR - bilateral hilar adenopathy hallmark of sarcoidoisis
hypercalcemia
hypercalciuria
biopsy
noncaseating granulomas
PFT
dec lung volume
dec diffusing capacity
dec FEV1/FVC ratio
ace enzyme levels just to note ds progress
stages of sarcoidoisis on chest xray
Stage I
bilateral hilar adenopathy without parenchymal infiltrates (highest rate of remission)
.
StageII
hilar adenopathy with parenchymal infiltrates
StageIII
diffuse parenchymal infiltrates without hilar adenopathy (least favorable prognosis)
.StageIV
pulmonary fibrosis with honey combing and fibrocystic parenchymal changes
treatment of sarcoidoisis
corticosteroids
hallmark of sarcoidoisis
bilateral hilar lymphadenopathy
causes of egg shell calcification
silicosis
sarcoidoisis
treated lymphoma
amyloidosis
chest xray finding of asbestosis
typically involves lower lobes
pleural plaques
chest xray finding of silicosis
typically involves upper lobes
and causes pleural plaques
occupational increasing risk of silicosis
sandblasters
quartz
mining
most common cancer caused by asbestosis
bronchogenic carcinoma
then malignant mesothelioma
biopsy finding of asbestosis
dumbbell shaped asbestos bodies
asbestosis increases risk of
bronchogenic carcinoma
malignant mesothelioma
silicosis increases risk of
TB
part of lung affected by asbestos
lower lobes
part of lung affected by silicosis
upper lobes
caplan syndrome
CWP + rheumatoid nodules in lung
modified wells criteria
clinical decision rule for suspected acute pulmonary embolism
symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy
score <4 less likely PE
score>4 indicates PE
modified wells criteria
clinical decision rule for suspected acute pulmonary embolism
symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy
score <4 less likely PE
score>4 indicates PE
modified wells criteria
clinical decision rule for suspected acute pulmonary embolism
symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy
score <4 less likely PE
score>4 indicates PE
why warfarin causes skin necrosis
warfarin inactivates protein C more quickly than 2,7,9 ,10 factors
thus creating a hypercoaguable state earlier leading to skin necrosis
so heparin is given for first few days with warfarin so tht it effect can come and then warfarin continued alone for 6 months
treatment of Pulmonary embolism
if pt is hemodynamically if pt is hemodynamically
stable unstable
⬇️ ⬇️
IV heparin thrombolytic therapy ie
1-2 wks streptokinase
⬇️ ⬇️
anticoagulate anticoagulate with
with heparin and warfarin for heparin and warfarin
6mths
⬇️ ⬇️
if C/I IVC filter if C/I IVC fillter + pul
embolectomy
diagnosis of pul embolism
non specific test
ABG levels
A-a gradient
usually elevated
CXRay
hamptom hump
westermark aigm
ecg- S1Q3T3 wave
sinus tachycardia
specific test
venous duplex USG
helpful when positive but not when negative
V/Q perfusion scan
has been replaced by CT SCAN
DONe when CT SCAN IS c/i
spiral CT test of choice
disadv - may miss small segmental clots
cannot be used in renal insufficiency due to contrast
pulmonary angiography is the gold standard
D dimer if normal them PE less likely
gold standard for PE
pulmonary angiography
test of choice for PE
spiral CT
risk factors for DVT
age > 60 yrs
malignacy
prior history of dvt
hereditary hypercoaguable states protein C ,S
prolonged immobization
obesity
cardiac ds
nephrotic syn
due to loss of antithrombin 3
major surgery
pregnancy and use of ocplupus anticoagulant
antiphospholioid antibody syndrome
has elevated PTT it does not mean tht it will increase bleeding
it is a lab finding because of antiphospholioid antibody and use of phospholipd to calculate it
false + ve VDRL
can cause both venous and arterial thrombosis
instead it is a hypercoaguable state
spontaneous abortion occur
triad of fat embolism
acute dyspnea
petechiae over neck
confusion
treatment of fat embolism
supportive with O2
dont use heparin and coumarin
hamptons hump
Hampton humprefers to a dome-shaped, pleural-based opacification in the lung most commonly due topulmonary embolismandlung infarction(it can also result from other causes of pulmonary infarction (e.g. vascular occlusion due toangioinvasive aspergillosis). While a pulmonary embolism is expected to result in a wedge-shaped infarction, the expected apex of this infarction may be spared because of collateral supply from the bronchial arterial circulation, leading to the characteristic rounded appearance of a Hampton hump.
westermark sign
focal oligemia seen in pulmonary embolism
new 2012 berlin defination of ARDS
acute onset < 1week
bilateral infilterates on chest imaging
pulmonary edema not explained by fliud overload or CHF
abnormal pao2/ Fio2 ratio
treatment of Obstructive sleep apnea
Obstructive sleep apnea - weight losss
CPAP
surgery reserved for last uvuloplasty
treatment of central sleep apnea
acetazolamide
progesterone
types of lung cancer
small cell
non small cell
large cell
squamous cell
adenocarcinoma
brochoalveolar carcinomasuperior vena cava syndrome
Obstruction of SVC by mediastinal tumor
facial fullness
face and arm edema
dilated veins over anterior chest arms face and jugular venous distention
SVC syn with confusion, blurring of vision is a oncologic EMERGENCY
signs of local invasion of lung cancer
svc syndrome
phrenic nerve paralysis
horner syndrome
unlateral anhidrosis
miosis
ptosis
pancoast tumorpancoast tumor
superior sulcus tumor
apical tumor involving C8 T1-T2 nerve root causing shoulder pain radiating down the arm
causes pain
upper extremitiy weakness
paraneoplastic syns with lung cancer
#occuring with SCC
SIADH
Ectopic ACTH
eaton lambert
#occuring with squamous cell carcinoma
PTH like hormone
hyoertrophic pulmonary osteoarthopathytreatment for NSCLC
surgery and radiation
treatment of SCC
chemo and radiation
