Pulmonology Flashcards
CDC criteria for ventilator associate pneumonia
Mech Vent for at least 2 days and
- Worsening gas exchange
- Radiographic evidence (infiltrate, consolidation, cavitation, pneumatocele)
- Three of the following
- temp instability
- WBC <4K or >15 K, bands >10
- cough
- sputum/ inc secretions
- apnea/ inc WOB
- wheezing, rales, rhonchi
- HR <100, >170
Most common organism with vent assoc pneu
Pseudomonoas
Enterobacter
Klebsiella
Staph aureus
Risk factors for VAP
BPD
Sedation
reintubation
Bld transfusion (inc pul edema)
acid suppressive med
ETT (reservoir bactaria, impedes physiologic clearnace)
Surfactant deficiency
Preventive measure for VAP
hand hygiene
closed ventilator circuit (avoid unnecessary equipment change/ disconnection)
dec standing water within the circuit
Management for suspected VAP
Linzolid/Vanco plus Pip-Taz/gent
severe cases: antipsuedomonal: cefepime/ceftaz, carbapenem
What is main mechanism of gas exchange in HFOV
Diffusion (there is constant entry of fresh gas)
Other mechanisms:
taylor dispersion, regional variation of turbulent and laminar flow, pendelluft movement
What is main mechanism of gas exchange on conventional vent and normal human ventilation
Bulk convective gas movement (actual entry and exit of gas through the patient= tidal volume)
Forces need to overcome for ventilation to happen
- Resistance
- Imepdence (mechanical barries to flow)
* R= 8nl/r4 - Can affect flow (length of ETT, diameter of ETT) in terms of HFOV decrease MAP in distal airway
What is primary risk factor for BPD
invasive mechanical ventilation
Stage of lung development for extremely premature infant
Canalicular stage
- set up for shear force injury (inc volutrauma with dec GA)
Strategies for invasive ventilation for extremely premature infant
- Limit tidal volume (avoid volutrauma)
- Optimal MAP and PEEP for alveolar stability (avoid atelectrauma)
- Minimizing oxygen toxicity
Effects antenatal steroids in fetal lungs
- Accelerate maturation of type II alveolar cells for surfactant production
- Increased thinning of alveolar septa
- Accelerated invasion of capillaries into the airspaces
Benefits of antenatal steroids
For infants between 22 and 25 weeks GA
reduces: mortality (39 to 18%), severe IVH, neurodevelopmental impairment
Benefits of SIMV vs nonsynchronized
- improves gas exchange
- inc pt comfort with dec need for sedation and muscle relaxation
- dec WOB, risk for barotrauma, volutrauma and IVH
- faster weaning
Settings for pressure limited vent
PIP: provide chest wall excursion
- needs PIP to manual adjusted with change in pulmonary dynamics
Settings for volume controlled
Desired tidal volume is set
- PIP automatically changed with change in pulm dynamics
- challenge if with air leak
TV for Preterm RDS <700 g
5.5–6 mL/kg 24 cm H2O
Rationale: Dead space of the flow sensor/decreased compliance, risk of air leak
Advantage of Volume targeted ventilation over pressure limited ventilation
Reduction of:
- in death or BPD at 36 weeks’ gestation
- duration of mechanical ventilation,
- air leaks
- hypocarbia
- grade 3 to 4 IVH as well as PVL and/or severe IVH
Initial setting for VTV based on wt/GA
What is the mechanism of gas exchange in HFJV
Taylor dispersion
Rationale for pressure support during weaning from conventional vent in extremely preterm infant
Unable to generate adeq TV, effective alveolar vent during spon breaths
- Poor lung compliance
- Increased airway resistance from the ET
- Inc chest wall compliance
Risk factors for TTN
Maternal:
- before completion of 39 weeks gestation
- CS without labor
- GDM
- maternal asthma
Fetal:
- male gender
- perinatal asphyxia
- prematurity
- SGA/LGA
What is responsible for fetal lung fluid
Chloride channels
- Volume of fetal lung is maintained by the larynx, which acts as a one-way valve, allowing only outflow of fluid
How is fetal lung fluid is reabsorbed
- through ENaC
- activated with onset of labor: maternal epinephrine and glucocorticoids
- ENac is found in apical membranes of type II pneumocytes.
- starling forces and thoracic squeeze(minor role)
Effect of neck position in ET position for infant <1kg
- neck flexion: decrease lip-to-carina distance by up to 1.5 cm,
- neck extension: increases the distance by up to 1.3 cm.
What is arterial oxygen content (CaO2)
CaO2 = (1.36 mL/g × Hb g/dL × SaO2) + (PaO2 mm Hg x 0.003 mL/[dL × mm Hg])
For every gram of Hgb, it carries 1.36 ml of O2
SaO2 in decimal
In lung development, what is responsible for branching of the mesoderm
Mesenchyme
Embryology:
Where is the respiratory tract derived from?
Endoderm
Forms from the ventral bud of the esophagus
Lung development is dependent on:
- fetal lung fluid
- Fetal breathing efforts
- Peristalsis of the airway
Origin of the pulmonary vasculature
6th aortic arch
* Pulmonary arteries : intrapulmonary structures for gas exchange
* Bronchial arteries: fr aorta supplies conducting airways, visceral pleura, connective tissue, pulm arteries
How does does pre-acinar arteries develop
Angiogenesis
new vessels from preexisting
supplies airways incl non resp bronchioles
How does does Intra-acinar arteries develop
Vasculogenesis
de novo from mesoderm
- supplies respiratory brochioles and alveolar ducts
- growth with alveolar devt
True or false:
fetus has greater vascular wall thickness vs adult
True
In terms of total vessel diameter
- Fetal pulm arteries has smooth muscles until preacinar
- Fetal to near term: Intra-acinar arteries lack muscle (all vessels around alveoli)
- In adults: all have smooth muscles but thin
How many alveoli present at birth
50-150M
Adults: 200-600M
Inc in alveolar phase until 3-8 yrs
Enhanced by Vit A and thyroxine
Delayed by steroids, O2, NTN def, MV, insulin, inflam
When are adult airways completed?
24 wks gestation
Pulmonary embryology
Embryonic stage:
a. Structural dev’t
b. abnormality
0-5 wks
a. Upper airway, tubes (until 5 lobes)
b. TEF, bronchogenic cyst
Pseudoglandular
a. Structural dev’t
b. abnormality
6-15 wks
a. Up to terminal bronchiole, separation of thorax and peritoneal cavity
b. CPAM, Cong emphysema, diaphragmatic hernia
Canalicular
a. Structural dev’t
b. abnormality
16-25 wks
a. Bronchioles, pneumocytes II to I
b. Pulm hypoplasia, surf def, alveolar cap dysplasia
Lung is viable
Saccular
a. Structural dev’t
b. abnormality
26-35 wks
a. multiple sacs fr terminal bronchiole; gas exchange via alveolar-capillary membrane
b. pulmonary hypoplasia, surf def
Alveolar stage
a. Structural dev’t
b. abnormality
36wks- 8y/o
a. alveoli inc, microvascular growth and vessel maturation
b. pulmonary hypoplasia, surf def, pulm HTN
Difference of Type I and II pneumatocytes
what is volume of fetal lung fluid
20-30 ml/kg
same as FRC
production near term 4-5 ml/kg/hr
How is fetal lung fluid produced
Cl actively out in the future air space
Inhibited by epinephrine, beta adrenegic agonist
cough it out
How is fetal lung fluid absorbed/ cleared prenatally
- dec FTF
- eNac
- Inc lymphatic oncotic p
Absorb sodium
suck in
How is fetal lung fluid absorbed/ cleared during labor
- mechincal forces
- catecholamine surge- eNac
- higher cortisol and thyroid- eNac
How is fetal lung fluid absorbed/ cleared postnatal
- lung distend: inc transpulm pressure
- inc lymphatic p
What is the most active component of surfactant
Dipalmitoyl Phophatidylcholine (DPPC) 50%
Surfactant can be deacivated by
Alveolar edema fluid
Meconium
In L/S ratio which substance reflects lung maturity
Lecithin
increases with gestational age
L/S ratio >2 lung maturity
Another test for lung maturity: Phosphatidylglycerol (not necessary of normal surfactant function)
What is Laplace’s law
P=2T/r
Plays role in surfactant by decreasing surface tension resulting in better compliance
What law is involved in air movement into the lungs
Boyle’s Law
* pressure of gas decreases as volume increases
P1V1=P2V2
What happens to the muscles of respiration during:
a. Inspiration
b Expiration
Chest wall and diaphragm
a. Contract
b. Relax
It is a reflex that prevents over inflation
Hering Breuer Inflation Reflex
There is an increase in this reflex as volumes increase above FRC, limits inspiratory duration
- reason decrease in RR with CPAP
This reflex helps maintain FRC, prevents atelectasis and involved in “sigh” breaths
Hering Breuer deflation reflex
- In pneumothorax d/t decrease TV, there is an inc in RR
- activity inverse with GA
This reflex is important during the first few breaths after delivery
Paradoxical reflex of head
inhibits hering breuer reflex, results in inspiration extended
Control of respiration
CSF: includes metabolic acidosis
No O2 receptor in central
Blood: dec O2, carotid and aortic bodies
Formula for alveolar ventilation
(TV-Dead space) x RR
Dead space usually 1/3 of TV
change in TV and RR is proportional to alveolar vent and pCO2
What is dead space
Space with no gas exchange
1. Anatomic- Upper airway
2. Alveolar- alveoli not involved in gas exchange
3. Physiologic= Anatomic + Alveolar dead space (also known as wasted ventilation)
= TV x (arterialCO2-expired CO2)/arterial CO2
- Bronchoconstrict- dec dead space, bronchodilate- inc dead space
- d/t shunting, abN vasculature
What lung zone does the neonatal lung behave
Zone 3
Pa>Pv>PA
zone 1- alveolar dead space- MAS, inc pressure
zone 4 no ventilation- PDA, pulmonary edema
What is A-a gradient
[FiO2 (barometric-H2O p)]- CO2/R- paO2
Barometric= 760
H20= 47
R= 0.8
-If A-a>600 for 8-12 hrs ECMO
Formula oxygen delivery
CO x [(1.34xHgbxO2 sat)+0.0003 paO2]
N 150-170 ml/kg/min
Factors that affect O2 del- CO, SV, Hgb, O2 sat, PaO2
SV- preload, afterload, contractility
What principle explains oxygen consumption
Fick Principle
- O2 consumption is the difference bet O2 del to tissues and the O2 returning from the tissue
- O2 consump= VO2= CO x1.34x Hg x (Arterial-venous O2 sat)
- O2 delivery dec what happens?
inc blood flow (dilation of capillaries)
Factors to increase oxygenation in assisted ventilation
- FiO2
- MAP
1. PEEP
2. PIP
3. I time
4. Flow
Caution: PEEP >6- not efficient
Inc MAP risk for overdistension
Inc I time- pneumothorax
How to inc tidal volume
Inc pressure gradient (Inc PIP or dec PEEP)
Tidal volume is independent of I or E time
Acute respiratory deterioration in ventilated neonates
- Displacement- include malposition
- Obstruction- secretions
- Pneumothorax
- Equipment
Think DOPE
If none of the above- IVH, seizure, hypoglycemia, hypotension, sepsis
Formula for Oxygen Index
(MAP x FiO2)/ paO2 x 100
>25 severe disease
Based on Poiseulis law, what affects resistance
Risk factors of TTN
- Delivery before 39 wks
- CS without labor
- Prematurity
- Male
- LGA/SGA
- Perinatal asphyxia
- M asthma
- GDM
CXR of TTN
- fluid in the interloabr fissure
- bilateral alveolar and interstitial edema
- prominent pulmonary vascular pattern with inc hilar markings
- lung hyperinflation
- Clears after 24 hrs
BG: mild hypoxemia and hypocapnia
* if hypercapnea- think of fatigue or air leak
It might not be TTN
- Differential cyanosis: PPHN, CHD
- Persistent tachypnea >4 days
- Rule of 2 hrs- not getting better, FiO2 >0.4
Prognosis of TTN
- Associated with asthma (inc if delivered via CS)
- Malignant TTN- develop PPHN
- Majority resolve 48 hrs
- No meds currently recommended
- All supportive
Benefits/Effects of Caffiene
- Improve minute ventiltion
- Improve CO2 sensitivity
- Dec periodic breathing
- Dec hypoxic resp depression
- Improve diaphargm activity
Long Term:
Dec Mech vent, dec BPD, Dec death, Dec CP, Dec congnitive delay
What is old BPD
Gross distortion of lung architecture due to oxygen toxicity and baro trauma
What is new BPD
Acquired developmental chronic lung disease that is a consequnece of premature birth; will have respiratory insufficiency
prevelance has not decrease over time
Based on GA
before 28 weeks up to 40%
before 24 weeks up to 80%
Based on BW <1000g: 16% with sBPD
Definition of BPD severity based on mode of support at 36 weeks PMA
Grade 1- <2LPM
Grade 2- Non-invasive vent (HFNC/CPAP)
Grade 3- Invasive ventilation
Does not anymore include FiO2
NIH- before 32 weeks, 28 days oxygen; severe BPD O2 >30% and/or pos vent at 36 wks
Pathophysiology of BPD
disorder of:
1. lung parenchyma- inc alveolar diameter
2. pulmonary vasculature- abn vascular devt
3. small and/or large airway dysfunction
less common finding- IV- gross distortion of lung architecture- large cystic area, fibrosis atelectasis, hyperinflation
It characterized by episode of acute and severe hypoxemia attributed to airway collapse or PPHN in a BPD patient
BPD spell
Goal: Open lung management through MAP and airway positioning- PEEP adjusted to mitigate airway collapse and hyperinflation to optimize compliance and dec resistance
Strategies for MV in BPD
- TV 8-13 ml/kg (d/t inc dead space)
- Inc PIP 30-40 (d/t poor compliance and high resistance)
- Slower rate <20/min
- Long IT >0.5s
- Pressure support for fast compartment
- PEEP 6-8 (d/t obstructive component, risk atelectasis, maintain FRC)
Same minute ventilation (TVxRR)
Goal of non invasive ventilation in BPD
Provide adeqaute support for growth and development and not avoid MV
Goal avoid: volutrauma, atelectrauma and O2 toxicity
red flags: poor growth, worsening PH, inability to tolerate developmentally appropriate physical activity, repeat hypoxic spells
Strategies for non-invasive vent in BPD
More reserved pacing of weaning (ie weekly/ twice weekly)
Goal: no significant tachypnea, WOB and able to participate in PT/OT activity
Pitfall: Inaqdequate support: worsen regional atelectasis and intermittent hypoxemia
This occurs when expiration is prolonged by high airway resistance and interrupted by subsequent inspiratory effort resulting in higher end expiratory volume (hyperinflation)
Auto-PEEP (PEEPi)
PE:
1. higher RR above the vent and mod-severe WOB (patient-vent asynchrony)
2. inspiration that do not trigger ventilator supported breath
When to consider tracheostomy
Unable to wean from NIV/MV as bby approaches or surpasses term-equivalent PMA
Has been associated with decreased resp suport, improved growth and participation in developmental activities in the short term
Outcome of sBPD and MV
- 97% free fr MV by 5 yrs
- Median age off MV 2 yrs
- Median age decannulation 3 yrs
d/t on going alveolarization
What are the approaches to prevent BPD
- Vitamin A
- Caffeine
Morbidities with BPD
- recurrent resp infection
- asthma
- neuro dev abN
- PPHN
Initial vent setting for CDH
- PIP: less than 25
- PEEP: 3–5
- rate of 40–60
- Paco2 50-70 mmHg.
what are the different congenital lung malformations
A neonate presents with expiratory stridor with feeding difficulty
Ba swallow showed at indentation on the esophagus
What is the most likely etiology?
Vascular ring most probably double aortic arch (40%)
due to right and left 4th brachial arches
What are the morbidity/mortality of congenital diaphragmatic hernia
- pulmonary hypoplasia
- abnormal pulmonary vasoreactivity
- Pulmonary hypertension
