All Flashcards
Which pneumocytes produce surfactant
T2
Max development of surfactant IuL
35th week
HMD treatment
Mild- CPAP
Severe- IMV+ surfactant replacement
Types and pathology of PAP
Impaired clearance of surfactant by macrophage
Primary- GMCSF Ab ( x macrophages)
Secondary- silicosis (x macrophages)
Investigations in PAP
BAL- Milky white/ PAS +
CXR- Diffuse fine reticulo-nodular infiltrates radiating from the hilum**
CT- CRAZY PAVING
MC bronchus for BXIS
Left main bronchus
(Horizontal, narrow—stasis of secretions-inflammation )
MC in babies
Mc lobe for aspiration overall/supine
RLL Superior»_space; RUL Posterior
Mc lobe for aspiration standing/sitting
RLL Posterior
Mcc if hemoptysis
TB
Mcc if massive hemoptysis
BXIS
Massive hempotysis criteria
> 150ml/ episode
> 400-600ml/day
Mccd hemoptysis
Aspiration of blood clot
Mx persistent hemoptysis
Brochial artery embolization
Resection of affected lobe
Pulmonary artery embolization (rare)
Pneumocytes having dividing capability
T2
Majority of pneumocytes
T2
Pneumocytes covering maximum area of lung
T1
Airway obstruction is prominent during?
Expiration (exp wheeze)
Inspiration is an active process- can overcome obstruction easily comparatively
Factors preventing collapse of alveoli
During expiration
Elastase—(a1 antitrypsin)
Surfactant
Emphysema features
Early- bulla, air trapped in alveoli/ inc RV FRC TLV
Late-Complete encircling of inflammation—decreased oxygen transport to blood
Ideal o2 flow rate and sat for COPD
1-2L/min
88-92%
Mechanisms of hypoxia
VP mismatch (emph/pte)
Shunt (cardiac/pulmonary)
(Pulm= pneum/ILD/Fibrosis/Atelectasis—damaged alveoli)
Diffusion defect (T1RF)
Hypoventilation(T2RF)
Rx for Intra pulmonary shunt/ damaged alveoli
IMV
Supplementary oxygen doesnt work
DLCO normal range and formula
Inhaled CO-Exhaled CO
70-90%
Alveolar conditions causing decreased DLCO
Emphysema
ILD
Fibrosis
Pneumonia
Blood conditions causing decreased DLCO
Anemia
PHTN
PTE
Increased DLCO?
PCV
Alveolar haemorrhage**
ASTHMA** (Eosiniphilic inflammation—increased NO production—inc vessel size)
Exercise
V/P ration is a measure of?
Max
Min
Alveolar oxygen tension
Max= apex
Min= base
(Max venti and max perfusion at BASE)
Tb 1° and 2° location
1= middle/lower zone (max ventilation)
2= apex (max v/q)
Volume at which outward recoil of chest equals inward recoil of lung?
FRC
FeV1 value
70-80%
FVC normal value
> 80%
PEFR significance
MEFR significance
P= flow in large airways (air first moves out of large airways) —-ASTHMA
M= average flow calculated during mid expiration (SMALL AIRWAY)—COPD/EMPHYSEMA
Measurement of RV
Helium dilution
N2 washout
Body plethysmograph ***
Obstructive LD spirometry
FeV1 decreases
FVC normal
RV = INCREASED***
Fev1/FVC = DECREASED
Restrictive LD spirometry
Fev1 DECREASED
FVC DECREASED
Fev1/FVC = normal/increased
Intrinsic RLD
Fibrosis
ILD
OLD
SARCOIDOSIS***
RV/TLC= normal****
(As alveoli gone)
Extrinsic RLD
Kyphoscoliosis
NM diseases (polio/GBS/MG/AL)
Diaphragm palsy
RV/TLC= INCREASES**
(RV normal/ TLC decreases)
Obstructive LD
Asthma
COPD
BXIS
Bronchiolitis
Breathing sounds in
Consolidation
Cavity
Large cavity
Tubular
Cavernous
Amphoric
Causes if rhonchi
Narrow lumen/free liquid/mucus
Asthma P. Edema COPD Foreign body Tumour
Increased vocal resonance is called
BRONCHOPHONY
Increased whispered sounds on steth?
PECTORLIQUOY
E—->A change in sound pronunciation
AEGOPHONY
Wheeze types
Monophonic- Tumor
Polyphonic- COPD/ Asthma
Wheeze heard mainly during?
EXPIRATION
If during inspirtation—severe obstruction
Coarse crepts cause
BXIS
Airflow into secretions
Fine crepts cause
ILD
Fibrosis
Pneumonia
P Edema
(Popping of alveoli)
Velcro crepts due to?
Interstitial FIBROSIS
Aka cellophane crackles/ Bi-basilar
Stony dull note present in
Plef
No push pull lesion with positive breath sounds
Consolidation
AIRBRONCOGRAM++
Cf of HYDROPNEUMOTHORAX
Straight line (not meniscoid)
Shifting dullness
Succusion splash
T1RF PAO2 PaO2 PaCO2 A-a
Normal
Decreased
Normal»increased (Good diffusion)
A-a= INCREASED
T2RF PAO2 PaO2 PaCO2 A-a
Decreased
Decreased
Increased (RESP ACIDOSIS)
Normal
T1RF causes
ILD
Alveolar flooding (pneumonia/ards)
Fibrosis
PTE
T2RF causes- Hypoventilation / decreased respiratory effort
COPD
Central : brainstem injury/ narcotics
Obstructive: COPD (mc) / FB
Peripheral: NMJ Diseases
Diaphragmatic injury
Rx RF
IMV (in T1)
NIV (T2)
C/I NIV
UNCONCIOUS***
Altered sensorium/ unco-op Cardiac arrest Hemo unstable Nasal sx Active GIBleed
ARDS Cardinal features
SOB
Hypoxemia
Pulmonary infiltrates
Reduced lung compliance
(HALLMARK= DAD)
Other names of ARDS
Shock lung
Blast lung
Traumatic wet lung
Direct causes of ARDS
FANTTS
Fat embolism Toxin Transplant (reperfusion injury) Near drowning Aspiration Severe Pneumonia
Indirect causes of ARDS
CABG High altitude Pancreatitis Narcotic poisoning Head injury Sepsis (mc) BT
Normal PCWP
6-12
Pcwp in Cardiogenic PE
> 18
Interstitial edema 18-25
Alveolar edema >25
Which never occurs in T1 RF
HYPERCAPNEA
Berlin criteria for ARDS
Acute SOB
Pul. Infiltrates
Non cardiogenic PE
PaO2/Fio2 < 300. Or. PaO2<60’mmHg
Criteria for Resp failure
PaO2 < 60
PaCO2 > 45
Types of RF
1 Hypoxic
2 Hypercapneic
3 Peri-operative-Atelectasis-GA
4 Shock (Hypoperf of resp muscles)
Mild mod sever ards criteria
PaO2/FiO2
200-300 = mild 100-200 = mod <100 = sev
Rx ARDS
Low TV MV (4-6ml/kg/min)
Adequate PEEP
Steroids
Newer Rx ARDS
ECMO
PRONE VENTILATION (12-16 hrs)- decreased diap compression of alveoli
Misc causes of ARDS
HELD
Hanging
Eclampsia
LF
Renal failure
Presentation time of PTE
cin 2 weeks
Predisposing genetic factors for PTE
Protein C S def
F5L mutation
Hyper- Homocystinemia
R/F PTE
DVT (estrogen pills)
Varicose veins
Trauma
Prolonged immobilization
Pregnancy
Malignancy
Nephrotic syndrome (AT3 excretion)
Lung pathology PTE
HEMOPTYSIS
Platelet thrombus—serotonin—BRONCHOSPASM
LUNG ISCHEMIA
(Pleuritis/Plef/dyspnea/tachypnea)
Mc sign and symptom of PTE
Sign TACHYPNEA
Syp DYSPNEA
Cardio Pathology of PTE
RVH—pushed septum in LV—decreased BP—shock
Cor pulmonale types
RV dysfn due to 1° resp cause excluding causes of keft heart
Acute—-PTE
Chronic- COPD (mc)/ ILD / CF / OSA / BXIS
CXR Findings of COR PULMONALE
Kerley B lines
(LAP > 20 then KBL++)
Prominent ULobe veins
Cardiac shadow
B/L plef
Well’s scoring PTE
SAPHHaI-C
Signs and symptoms = 3 Alternative Diagnosis no? = 3 Prior PE/DVT = 1.5 Hemoptysis = 1 HR> 100 Immobilisation > 3 days or Sx cin 3wk =1.5 Cancer =1
If >4 = CTA with contrast(IxoC)»_space;V/Q Scan
Low score Mx of PTE
D-dimer (95% sensitive)
If positive. CTA
Otherwise r/o PTE
ECG PTE
Mc= Sinus tachycardia
Msp= S1Q3T3
2nd Mc = inv T wave in V1-4
CXR PTE
Mc = normal**
WESTERMARK SIGN
(Focal oligaemia)
HAMPTON HUMP
(Wedge opacity)
PALLAS SIGN
(Dil. R descending Pul. Artery)
Other Ix PTE
ECG
CXR
LL usg (r/o DVT)
D-dimer
CTA (Ixoc)
INVASIVE PUL ARTERIOGRAPHY (GST)
V/Q scan (prenancy/RenalF/Contrast intol
Rx Massive PE
Shock+RV dysfn
500ml NS
Vasopressors
Anticoagulants
Definitive: Thrombolysis»_space; sx embolectomy
Rx submassive(RV dysfunction) and Minimal PE (normal RV and BP)
S= > 70 years = Anticoagulant—Tlysis
< 70 years = Thrombolysis
Mcc of preventable hospital death/ Mccd in post sx patient
Acute PE
Anticoagulant? Thrombolysis? (Drugs)
Heparin bridge warfarin
Heparin f/b dabigatran (DTI)
Xa inhibitors
Thrombolysis : Alteplase»_space; streptokinase
Rx Pul Edema
Furosemide + NTG sublingual (HR>100)
F + NE/DP (HR<100/ Shock -)
F + DOBUTAMINE (HR<100 / Shock +)
New tx for PTE
Catheter directed thrombolysis (CDT)