Dz States 3 Flashcards
bronchiectasis pathphys
severe viral infxn causes inflamed and easily collapsed airways = air flow obstruction, decreased clearance of secretions
therefore chronic bacterial growth resulting in inflammation and damage to bronchioles
bronchiectasis
persistent inflammatory injury causes
- permanent dilation of proximal and med. sized bronchi
- progressive inability to clear secretions and resolve colonization or repeat infection
- COPD
etiologies of bronchiectasis (7)
- infection
- bronchiole obstruction
- aspiration
- CF
- allergic bronchopulmonary aspergillosis
- AAT
- autoimmune/connective tissue
epidemiology of bronchiectasis
slender caucasian women, 60+
often cause by MAC
symptoms of bronchiectasis
cough and mucopurulent sputum production (months - yrs)
dyspnea, pleuritic chest pain, wheezing, fever, weakness and weight loss
exacerbations: increased and more viscous sputum with would odor
signs of bronchiectasis
blood-streaked sputum but few specific signs
rales, wheezing, and rhonchi
evaluation of bronchiectasis
discovering cause and tx underlying dz
spirometry irreversible obstruction (no change with bronchodilators)
sputum smear culture (infectious organisms)
HRCT scan of chest with contrast = SOC
tx of bronchiectasis
early recognition of bronchiectasis and tx underlying cause
ABX and chest physiotherapy (Abx 1/wk)
+/- bronchodilators, corticosteroid tx, dietary supplementation, oxygen or sx therapies
pulmonary HTN
increased resistance thru lung is present = vascular remodeling occurs and pt develops HTN
PA pressure > 25 mmHg
PAH pathophys
vascular scarring, endothelial dysfunction and intimal/medial smooth muscle proliferation (decreased lumen size)
vascular remodeling causes RV hypertrophy then RV dilation/RSHF symptoms, decreased preload
etiologies of PAH
- sporadic/idopathic, hereditary
- Pulmonary artery muscle dz (connective tissue dz - scleroderma, SLE, HIV, HTN, anemia
- Drug and toxin
- LV dysfunction, valve dz
- hypoxemia lung dx (COPD, OSA)
- PE
drugs that may cause PAH
st. john’s wort
SSRIs
cocaine, meth
medical disorders that may cause PAH
HIV, liver dz, hemolytic anemia
PAH pathophys
- high pressure pulm circuit = pulmonary vascular remodeling
- RV hypertrophy to maintain output in face of increased resistance
- pull remodeling = RV failure
pathogenesis of PAH
progressive hypoxemia, hypercapnia, acidemia
excess peripheral oxygen extraction and eventual erythrocytosis
PAH s/s
initially vague fatigue, and decreased exercise tolerance
exertional dyspnea
lungs are clear (blood backs up to periphery)
diagnosing PAH (imaging)
2D trans thoracic can screen in high risk pts (can tell if increased pressure is there)
R sided cath is GOLD stnd for evaluation
HRCT scan
V/Q scan
anatomy changes of PAH
visible on 2d echo
increased pulmonary pressure
dilated RA and RV hypertrophy
R –> L shunt across PFO
R Cardiac Cath
specifically quantifies RV and LV function
excludes valvular disease and measure pulmonary vascular resistance
can also det. if reactive to CCB
who do we give a full PAH work up
LV dysfunction, COPD = work up stop after confirmation 2D echo
absent or insufficient: Lab eval (HIV, autoimmune, LFTs), PFT, polysomnography, V/Q scan
tx of PAH
tx begins early, det. underlying dz
- Diuretics (fluid retention, decrease pulmonary and hepatic congestion and edema)
- supplemental O2
- consideration of anticoagulation
- exercise
- digoxin (RV EF but more sensitive to dig toxicity)
advanced PAH tx
synthetic prostacyclin analog (vasodilators inhibit platelet aggregation)
endothelin receptor agonists (blocks vasoconstriction)
nitric oxide GMP enhancers (Oral PDE-5 , guanylate cyclase)
CCB
surgical options for PAH tx
atrial septostomy (create the R/L shunt )
transplant
diseases of disordered breathing
Pickwickan syndrome (sig CO2 retention, can’t take deep breaths)
Central apnea (neural issue causes decreased respiratory drive, tumor/stroke)
obstructive apnea (something wrong when relaxed - ok during day)
OSA
relaxed tissue of mouth and pharynx occlude air passage as pt tries to breath
causes of OSA
anatomical features (macroglossia, tonsils, hypertrophy, acromegaly, etc)
sedatives
other risk factors (DM, lung dz)
typical OSA pt
men > women, older, younger AA male
craniofacial issues, heredity, current smoking, nasal congestion
obese male, HTN
clinical features of OSA
STOP BRAG
Snore loud
Tired/fatigued
Observed stop breathing
Pressure (HTN)
Bmi >35
Age > 50
Neck circumference >43
Gender = male
diagnosis of OSA
polysmonography/sleep study
CBC
exclude drug use
study findings: decreased pulse ox, tachycardia, arrhythmia (VTACH), increased BP
mild OSA
asymptomatic, report sedentary sleepiness
noted only in retrospect
respond to tx
moderate OSA
take steps to avoid daytime sleepiness
likely HTN but no co pulmonate manifestations
respond to tx
severe OSA
freq. manifestations of car pulmonate
all need tx
not benefit for symptoms and dz
tx of OSA
weight loss, avoidance of alcohol/sedatives
CPAP +/- O2 (difficult mask, remind pt that symptoms can be deadly)
UPPP
what does effective lung function req. ?
patient, dry alveoli
small amount of interstitial fluid
appropriately perfusion of capillaries
diffuse disruption of fluid balance cuisine leaky capillaries and proteinaceous deposit
ARDS/ALI
ARDS clinical criteria
- Acute onset
- Bilateral infiltrates
- No decrease in LA pressure (just lungs)
- PaO2/FiO2 ratio <200
etiologies of ARDs/ALI
Sepsis aspiration PNA severe trauma drug overdose massive tranfusion/transplant EtOH
pathophysiology of ARDS
- inciting event
- pro inflammatory cytokines released (TNF, IL-1, IL-6, IL-8) and neutrophil recruited to lungs = damage to capillary and alveolar endothelium
- protein escapes from vascular space
- osmotic gradient for reabsorption is lost and fluid pours into intersitium
- alveoli fill with bloody, proteinaceous fluid and cellular debris
- surfactant loss, alveolar collapse
- V/Q mismatch and hypoxemia
- loss of lung compliance
- respiratory failure
clinical picture of ARDS
acutely ill within 48-72 hrs after inciting event
tachypnea, tachycardia, refractory hypoxemia, acute respiratory alkalosis
intubation/ventilation
diagnostic eval of ARDS
ABG shows hypoxemia despite 100% O2 and alkalosis
CXR - diffuse, fluffy infiltrates, air bronco grams
Lab studies - leukocytosis, DIC, lactic acidosis
initial course of ARDS
IF survive initial:
severe pulmonary edema that slowly improves
req. prolonged mechanical ventilation due to hypoxemia
* some pts do not improve = honeycombing
subsequent ARDS course
prolong ventilation req and patients are at risk for many complications
Barotrauma, pneumothorax (stiff lung = tension pneumothorax)
noscocomial PNA
DVT/PE
GIB
sedation and paralysis
mortality from ARDs
mortality improved with better supportive care
death form respiratory distress is uncommon
precipitating event causes death in first few days, nosocomial infection and sepsis cause death
respiratory distress syndrome
neonatal equivalent of ARDS
deficiency of surfactant production either due to premature infant or genetic/birth
alveolar development
lungs grow in late gestation and 2+ yrs after brith
zero alveoli at 32 weeks, 50-150 million at term , 300 million adult
surfactant development
Type II growth begins at week 20, surfactant production during weeks 34-36
amniotic fluid tested for present of lectin to determine lung maturation
fetal stress and surfactant production
decreased due to hypoveolmia (mother), hypothermia, acidosis, hypoxemia, genetic disorder
pathophys of respiratory distress syndrome
- instability at end exhalation, decreased compliance, low lung volumes = atelectasis
- lung inflammation and epithelial injury, extravasation of fluid and pulmonary edema
- pulmonary shunt and hypoxemia - lung perfused but not ventilated
risk factors respiratory distress syndrome
prematurity
previous premie, fetal distress, maternal FM, asphyxia
respiratory distress syndrome exam
cyanosis tachypnea nasal flaring intercostal/sternal muscle retraction grunting
respiratory distress syndrome CXR
atelectasis
ground glass haze
clinical course respiratory distress syndrome
during first 72 hrs increasing respiratory distress and hypoxemia
edema, apnea, respiratory failure
uncomplicated show spontaneous improvement
prevention and tx of respiratory distress syndrome in MOM
prevent pre term delivery
neonatal cold stress, asphyxia and birth , hypovolemia
if unavoidable - antenatal corticosteroid, stimulates surfactant
tx of baby respiratory distress syndrome
exogenous surfactant administration
warm O2 + monitoring
empiric IV ABx
