Pulmonary Flashcards
What are some key differences of pulmonary vessels compared to systemic vessels?
- Larger diameters
- Shorter, more branches
- Higher # of arterioles
- Arterioles do not direct flow
- Lower resistance from lower resting muscle tone in arterioles
What occurs to pulmonary vessels during exercise?
Increased cardiac output leads to a decrease in resistance and increase in blood flow: recruitment and distension
How does lung volume affect vascular diameters and resistance?
Alveolar vessels are compressed at higher lung volumes, which increases R
Extra-alveolar vessels are pulled open by expansion of attached parenchyme, which decreases R
Results in a drop in total R followed by an increase
What is hypoxic vasoconstriction?
Constriction of pulmonary vessels below avleolar PO2
What three things affect intravascular pressure (Piv)?
Cardiac cycle - high compliance system does not dampen pulse
Vertical position - gravity leads to high Q at base, low Q at apex
Respiratory cycle - Inspiration: PA Patm
What is the relationship of arterial, alveolar, and venous pressure in the three zones (of West)?
Zone 1: Above LA, decr. Piv.; alv. capillaries crushed –> low Q
PA > Pa > Pv
Zone 2: At LA; arterioles dilated but venules squeezed leading to incr. R and low Q
Pa > PA > Pv
Zone 3: Below LA, causing incr. Piv; Ptm along vessel dilates it causing decr. R
Pa > Pv > PA
How is left atrial pressure measured?
Swan-Ganz catheter threaded through R heart to pulm aa., measuring pulmonary capillary wedge pressure (PCWP), usually 7-8mmHg
What determines the rate of fluid flux out of capillaries?
According to Starling’s Law:
- Difference in capillary and interstitial hydrostatic P
- Difference in oncotic pressure of lung interstitium and plasma multiplied by the reflection coefficient of the membrane
What is Poiseuille’s equation and how does it relate to pulmonary hypertension?
Ppa = Q x PVR + PCWP
The difference in P b/t the pulmonary a. P and left atrial P depends on the blood flow and pulm. vascular R
What are some causes of pulmonary HTN?
Incr. Q: L to R shunts
Incr. Rp: hypoxic vasoconstr., clot, tumor, inflammation
Incr. left atrial P: left ventricular cardiomyopathies, valvular dz
What happens in fetal circulation after birth?
Ductus arteriosus, foramen ovale close due to decr. in R atrial P
Fetal pulm. circulation incr. P due to incr. PO2 and PGI2/PAF
How does PCWP cause pulmonary edema?
When PCWP > 18-25mmHg, fluid moves from the capillaries into the interstitium. If the rate of clearance is exceeded pulmonary edema (interstitial first, then alveolar) will occur
What are the steady state values of PAO2/PaO2 and PACO2/PaCO2? How are these calculated?
PAO2 = 104mmHg PACO2 = 40mmHg PaO2 = 100mmHg PaCO2 = 40mmHg
Pressure of a gas in air present in alveoli (Pi) depends on humidity (PH2O) and the total P of inspired air
Pi = (Ptot - PH2O)(%Pi)
What is anatomic dead space? How can it be measured?
The 150mL of inspired air that remains in the conducting airways after each breath.
Measured by Fowler N2 washout method: pt inhales 100% O2, exhaled air is analyzed for N2. N2 in dead space mixes with inhaled O2
What is physiologic dead space?
VD(phys) = VD(anat) + VD(alv)
Proportion of dead space in each breath:
VD/VT = (PACO2 - PTCO2) / PACO2); normally ~30%
How is alveolar ventilation measured?
Alv V: flow of air into alveoli taking part in gas exchange; must be sufficient for CO2 removal, so PACO2 ~ VCO2 / VA
VA = 0.863 (VCO2 / PACO2)
How do parasympathetic and sympathetic NS affect airflow?
Para: bronchoconstr
Sympa: bronchodilates
Act via increasing [cAMP] in smooth muscle cells
What is vital capacity?
VC = ERV + IC VC = ERV + VT + IRV
Max. vol. of air that can be expelled after a maximal inspiration
What is residual volume?
RV = FRC - ERV
Volume of gas remaining in lungs after forced expiration
What is expiratory reserve volume?
Volume of air beyond normal tidal volume that can be forcibly expired
What is inspiratory reserve volume?
Volume of air beyond normal tidal volume that can be forcibly inspired
What is functional residual capacity?
FRC RV + ERV
Volume of gas remaining in lungs after tidal expiration; cannot be directly measured
What two factors contribute to lung collapsibility?
Alveolar surface tension: surfactant lowers T when r reduced, preventing collapse of smaller alveoli into larger ones
Elastic fibers: alveoli tethered by fibers in interstitium tend to pull and hold alveoli open - lowers R – radial traction
What is the differential diagnosis for obstructive lung disease?
F - foreign body A - asthma C - chronic bronchitis/bronchiectasis E - emphysema S - small airway disease
What is the PFT hallmark of obstructive lung disease? Emphysema? Chronic bronchitis?
Decr. FEV1 Decr. FVC Decr. FEV1/FVC Incr. TLC Decr. DLCO
What is the differential diagnosis for restrictive lung disease?
P - Pleural disease A - alveolar filling disease (ARDS) I - Interstitial lung diseases N - neuromuscular T - thoracic cage abnormalities (kyphoscoliosis)
What PFTs are indicative of restrictive lung disease?
Decr. FEV1 Decr. FVC Incr. or nl FEV1/FVC Decr. or nl FEF25-75 Decr. TLC Decr. FRC Decr. DLCO
What is compliance and how is it affected by increasing volume?
Change in volume as transmural pressure is changed
∆V / ∆Ptm
Compliance decr. as volume incr. and walls approach maximum stretch
Why does the slope of the compliance curve differ from inhalation to exhalation? What is this called?
Greater P is needed to open a previously closed airway than to keep an open airway from closing. This effect is called hysteresis
How do restrictive and obstructive lung diseases affect lung compliance?
Restrictive - scarring causes incr. interstitial tissue, reducing compliance, incr. WOB
Obstructive - emphysema: destroy parenchyma, increasing compliance
Why is expiratory flow limited in COPD?
Loss of radial traction - airway collapse in expiration
Loss of elastic recoil - decr. alv. driving P
What factors affect normal PFT values?
Age - older lower
Sex - women lower
Race - blacks lower
Height - shorter lower
How are flow volume loops changed in disease states?
Obstructive: shifted left, characteristic “scoop” on expiration, reduced total flow
Restrictive: Normal shape, shifted right, reduced total flow
What determines the diffusion of a gas across a membrane?
Gas solubility, pressure difference, area of diffusion, thickness of membrane
Diffusion ~ (A x G x ∆P) / T
Why do O2 and CO2 diffuse at similar rates in the lung?
Driving force for diffusion is ∆P. Since ∆PO2 > ∆PCO2 (60mmHg vs. 6mmHg) they diffuse similarly
How are diffusion and perfusion capacities measured?
Diffusion: DLCO - measures ability of CO to cross into bloodstream independent of blood flow
Perfusion: N2O - amount taken up depends on blood flow and not barrier
How is the alveolar PO2 estimated?
PAO2 = PIO2 - (PaCO2/0.8) PAO2 = 150 - (PaCO2/0.8)
What is the Aa gradient, how is it calculated, and what is its significance?
The Aa gradient measures the difference in PO2 b/t alveolar gas and mixed arterial blood; a large Aa gradient indicates pathology of gas exchange (nl 5-10mmHg; or age x 0.3).
Aa = 150 - PCO2/0.8 - PaO2
Why does helium dilution underestimate lung volume in obstructive lung disease?
Helium doesn’t reach portions of the lungs distal to the obstruction
Why is diffused O2 so important for normal gas exchange?
Due to cooperative binding of O2 to Hb, the presence of extracellular O2 diffused in the plasma ensures that O2 is delivered where it is needed–small ∆ in SaO2 drastically changes Hb binding of O2
What is the equation for the amount of O2 carried in the blood?
CaO2 = (1.34 x Hb x SaO2) + (0.003 x PaO2)
Total amount carried by hemoglobin plus dissolved plasma O2
What factors occur in actively working tissue and how do they affect Hb binding O2?
Incr. tempr
Incr. PCO2
Incr. 2,3-DPG
Incr. acidity (decr. pH)
All 4 decrease Hb affinity for O2
What effect do drugs or chemicals such as nitrites and sulfonamides have on Hb? How is this dealt with?
Oxidize Hb to MetHb, which can’t bind O2. Reduced by MetHb reductase, so only 1.5% of Hb is in MetHb state
How is CO2 transported in the blood (3 forms)?
Dissolved CO2 (6%) Bicarbonate (70%) - carbonic anhydrase in RBCs Carbamino compounds (24%) - carbaminoHb formed by CO2 combining with free amine groups
What is the Haldane effect?
Oxygenation of blood decreases its ability to carry CO2
Deoxygenation of blood increases its ability to carry CO2
What is the equation to calculate alveolar O2?
PAO2 = FIO2 x (Patm - PH2O) - (PACO2 / R)
Normally 100mmHg
What are some causes of hypoxemia (6)?
V/Q mismatch (most common) Reduced DLCO (increased Aa gradient) Alveolar hypoventilation Reduced PIO2 (altitude) Reduced FIO2 (fire) Shunt (V/Q = 0)
What equation describes the relationship between arterial PCO2, CO2 production, and alveolar ventilation?
PaCO2 = K(VCO2 / VA)
The arterial PCO2 is proportional to the volume of CO2 produced by the tissues divided by the alveolar ventilation
What are four common causes of hypercapnia?
Alveolar hypoventilation (decr. VA)
Incr. VD/VT (rapid, shallow breathing)
Incr. CO2 production (w/ fixed ventilation)
Severe V/Q mismatch
How does the lung respond to high V/Q due to changes in perfusion?
Hypocapnic bronchoconstriction
VA is decreased to compensate for decreased blood flow. VA is increased elsewhere to accommodate increased Q caused by blocked vessels.
If Q is increased, VA is increased.
How does the lung respond to low V/Q?
Hypoxic vasoconstriction, in order to offset effects of shunt (hypoxemia)
What is a normal Aa gradient?
0-10mmHg, increases w/ age
When hypoxemia is present and PaCO2 is reduced, the Aa gradient MUST be wide
What interstitial lung diseases are associated with smoking?
Desquamative interstitial pneumonia (DIP)
Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD)
Pulmonary Langerhans cell histiocytosis (PLCH)
Idiopathic pulmonary fibrosis (IPF)
What is the DDx for interstitial lung disease that is granulomatous?
Sarcoidosis
Infection
Hypersensitivity pneumonitis
What part of the brain acts as a respiratory rhythm generator? What structure initiates inspiration?
The rostral VRG, the Botzinger complex. It contains pacemaker cells.
The DRG contains primarily inspiratory neurons that generate APs of increasing intensity: ramp signal
What structures in the brain modulate respiration and fine tune respiratory rhythm?
Apneustic center - prolong ramp action potentials
Pneumotaxic center - switch off inspiration, regulate inspiratory volume
What are the chemosensors in the aortic and carotid bodies, and how do they communicate with the DRG?
Glomus cells - depolarized by low PaO2, high PaCO2, and low pH. Signal DRG to increase ventilation
How do central chemoreceptors sense changes in pH?
Central chemoreceptors sense increase [H+], which is produced when CO2 diffuses across the BBB into the CSF, which reacts with H2O to form HCO3- and H+
What is the Hering-Breuer reflex?
Cessation of inspiration following signals from slowly-adapting pulmonary stretch receptors within the tracheobronchial tree when the lungs overinflate
What function do J receptors serve?
J receptors in the alveoli and small conducting airways respond to interstitial edema and engorgement of pulmonary capillaries. They mediate closure of the larynx and apnea followed by rapid shallow breathing. They also mediate tachypnea in response to PE
What is the main difference between OSA and central sleep apnea?
Both OSA and CSA have >5 apneic episodes/night but CSA is characterized by lack of respiratory drive during apneic episodes
What are the main advantages to inhaled treatments over systemic treatments for respiratory pharmacologic agents?
Delivery to respiratory tissues decreases systemic absorption and thus side effect profiles
The portion of inhaled drugs that are absorbed are passed through the liver and inactivated via first pass metabolism, thereby decreasing systemic side effects
What are the inhaled vasodilators and their mechanism of action?
NO - cause pulmonary vasodilation to acutely lower pulmonary arterial P; improves oxygenation but not survival in ARDS
Prostacyclin - causes pulmonary vasodilation; has anticoagulation/antiproliferative actions
What are the inhaled mucolytics?
N-Acetylcysteine (NAC) - breaks S-H bonds to break down proteins; can irritate bronchial mucosa and induce cough
DNase - breaks up DNA of degenerating neutrophils/bacteria in order to reduce sputum viscosity (not approved for chronic bronchitis)
What are the beta agonists and how do they work?
Stimulate beta-2 receptors, incr. cAMP levels via IP3, increasing Ca2+ efflux.
Albuterol (fast onset, short duration)
L-albuterol - B2 > B1, decr. side effects
Salmeterol (slow onset, long duration)
Formoterol (fast onset, long duration)
What are the anti-cholinergics and how do they work?
Block muscarinic receptors to block cholinergic mediated bronchoconstriction; better for COPD than asthma (due to increased musc. tone in COPD)
Ipratropium - short acting, blocks M1, M2, M3 receptors
Tiotropium - long acting, blocks M1, M3 receptors
How do anti-leukotrienes exert their effect?
Leukotrienes are involved in IgE mediated inflammation and bronchoconstriction; blocking LKTs cause a decr. in eosinophils and incr. in FEV1 in asthma
Zileuton - blocks 5-lipoxygenase
Montelukast/zafirlukast - blocks binding of LTE4 to receptors in lung tissue –> bronchodilation
What is the mechanism of PDE4 inhibitors, and for what condition(s) are they prescribed?
PDE4 inhibition increases cAMP levels in airway smooth muscle cells and inflammatory cells, leading to mild bronchodilation and anti-inflammatory effects.
Roflumilast - Rx in COPD exacerbations, but monitor liver tox.
How do inhaled steroids work to decrease inflammation? What are some examples?
Trigger eosinophil apoptosis, decrease mast cell degranulation and macrophage proliferation
Act on epithelial cells, decreasing cytokine and mitogen release
Bind to smooth muscle cells and mucus gland cells
Beclomethasone
Fluticasone
Budesonide
Mometasone
What are cromolyn and how does it work?
Blocks the release of histamine and LKTs from mast cells
Tx exercise-induced bronchoconstriction, limited use in standard asthma
Nedocromil is related but also blocks mediator release from eosinophils, macrophages, and platelets; used infrequently
What are anti-tussives?
Cough suppressants/expectorants
Codeine - act on mu receptor
Dextromethorphan - non-opiate with affinity for mu receptor, modest effectiveness
Benzonatate - local anesthetic in upper airway
Guaifenesin - draws free water into airway to assist sputum clearance
What causes expiratory flow limitation in COPD? In chronic bronchitis?
COPD - loss of radial traction leads to airway collapse; loss of elastic recoil results in decr. alveolar driving pressure
Chr. bronchitis - edema, smooth muscle constriction, incr. mucus production, mucus gland hyperplasia, inflammation –> incr. airway resistance
What treatment options are there for COPD?
Smoking cessation SABA - albuterol LABA - salmeterol LAMA - tiotropium (COPD > Asthma) Theophylline (systemic bronchodilator) PDE4 inh. Corticosteroids Surgery - reduce lung volume Pulm rehab O2 if hypoxemic
What are some causes of acute exacerbations of COPD? What treatments are available?
Bacterial infxn (most common) Viral infxn Environmental exposures (pollution)
Life threatening event, can result in permanent loss of lung fxn
Tx: Bronchodilators - SABA, LAMA, theophylline
Anti-inflammatory - systemic/inhaled corticosteroids
Abx
Alpha-1-antitrypsin
Immunization - influenza, pneumococcus
PDE-4 inh.
Expectorants/mucolytics NOT EFFECTIVE
What is the biggest factor that influences the development of asthma?
Atopy - predisposition toward developing hypersensitivity; may have genetic component
What are the hallmarks of asthma?
Airway inflammation Airway hyperresponsiveness (AHR) Airflow obstruction
What are the key factors involved in the early and late stages of asthma?
Early - bronchospasm - mast cells, and macrophages
Late - bronchospasm, edema, inflammation - recruitment & activation of eosinophils; cytokines (IL-4, -5, -13) released
What occurs during airway remodeling in chronic asthma?
Mucus gland hyperplasia
Angiogenesis
Subepithelial fibrosis
Airway smooth muscle hypertrophy/hyperplasia
What is aspirin induced asthma and how does it develop?
Aspirin inh. COX, incr. arachidonic acid pathway towards lipoxygenase pathway –> incr. LKTs –> edema, bronchoconstr., mucus, eosinophils
Tx: avoidance, standard asthma tx LKT modifiers (montelukast, zileuton)
How is methacholine used to dx asthma?
Asthmatics have incr. rxn at low conc. of methacholine - 20% reduction in FEV1 at low doses
Nl test in untreated pt r/o asthma; nl tests in treated pts
What are the key factors involved in the early and late stages of asthma?
Early - bronchospasm - mast cells, and macrophages
Late - bronchospasm, edema, inflammation - recruitment & activation of eosinophils; cytokines (IL-4, -5, -13) released
What infection are CF pts prone to get, and how can it be prevented?
Pseudomonas aeruginosa
Tx: inhaled tobramycin
What are the main differences between CF and non-CF bronchiectasis?
Non-CF: acquired disorder characterized by permanent dilation and destruction of bronchial walls; requires infectious insult plus impairment of drainage, airway obstruction, and/or defect in host defense
CF: pulmonary manifestation of a multi-organ dz
What is required for a CF dx in an adult?
Clinical sx consistent w/ CF in at least one organ system
Evidence of CFTR dysfunction
What are characteristic microscopic findings in asthma?
Bronchial smooth muscle hypertrophy Bronchial basement membrane thickening Bronchial wall edema/inflammation - eosinophils and mast cell infiltrate Goblet cell hyperplasia Submucosal gland hypertrophy
What are the two types of emphysema and how are they distinguished?
Panacinar - enlargement of airspaces in distal acinus initially, later whole pulmonary acinus is involved; lower lung zones more severely affected. Assoc. w/ alpha-1-antitrypsin deficiency
Centriacinar - enlargement of proximal acinar airspaces; emphysematous areas separated by relatively normal lung; more severe in upper lobes. Assoc. w/ smoking
What is the clinical definition of chronic bronchitis?
Productive cough for at least 3 months during 2 consecutive years w/o other known cause
Reid index increased - nl 0.4
Assoc. w/ smoking, often coexists w/ emphysema
What histologic changes are apparent in bronchiectasis?
Acute neutrophilic inflammation
Increased fibrosis - subepithelial collagen
Squamous metaplasia - ciliated –> cuboidal epithelium
What is the blood supply to the layers of the pleura? Lymphatics?
Parietal: systemic aa. and vv.; stoma drain pl. space
Visceral: bronchial aa. and pulmonary vv.; lymph drains towards hila, not involved in clearance of pl. space
What is the innervation to the layers of the pleura?
Visceral: None
Parietal:
Costal/peripheral - intercostal nn., pain referred to chest wall
Central - phrenic nn., pain referred to ipsilat. shoulder
Why is gas in the pleural space absorbed by venous blood?
Due to decreased pO2 in venous blood (40mmHg), the total venous P (by Dalton’s law) is 68cmH2O below Ppl
How is a transudate different from an exudate? How do they develop?
Transudate: plasma ultrafiltrate caused by either increased hydrostatic pressure or decreased osmotic pressure
Exudate: protein-rich fluid from capillary leakage secondary to inflammation or dz of pl. surface, independent of Starling forces
What are some major etiologies of transudative effusions?
CHF - RV (parietal transudate) or LV (visceral transudate)
Nephrotic syndrome
Cirrhosis
Atelectasis
What are some etiologies of exudative effusions?
Tumors - primary & metastatic Pneumonia - parapneumonic, empyema TB PE Collagen vasc. dz - lupus, RA Trauma
What is needed for an effusion dx - trans. vs. exud.?
Pl fluid protein / serum protein > 0.5
Pl fluid LDH / serum LDH > 0.6
or pl fluid LDH > 2/3 upper limit of nl serum LDH
How are pleural effusions treated?
Transudates: tx underlying cause, effusion should resolve
Exudates: tx underlying cuase but further intervention might be req’d
In pneumonia, thoracentesis indicated for effusion > 10mm
Chest tube drainage for empyema, complicated parapneumonic effusion
What are CXR findings indicating a tension PTX?
Contralateral shifting of trachea, mediastinum
Compressed lung w/ hypoopaque lung field
Depressed/inverted diaphragm
What are general physical exam findings in interstitial lung dz? CXR?
Cyanosis Tachypnea, tachycardia Clubbing Velcro rales, end-insp. squeaks Left parasternal heave, loud P2, right S3 LE edema
CXR: diffuse reticular infiltrates, honeycombing
What are some tx options for IPF?
Lung transplant
Nintedanib - VEGF-R, FGF-R, PDGF-R blockade - incr. exercise tolerance
Pirfenidone - inh. TGF-B expression
What are the ILDs of known etiology or association?
Pneumoconioses
- Asbestosis, coal worker’s pneumoconiosis, silicosis, berylliosis
Hypersensitivity pneumonitis
- Humidifier lung, bird fancier’s dz, farmer’s lung
Direct tissue injury
- Silo filler’s lung (NO2 exposure), RADS
Airway dz - occupational asthma
- Baker’s asthma
What are the idiopathic interstitial pneumonias?
Usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF)
Cryptogenic organizing pneumonia (COP)
Acute interstitial pneumonia (AIP)
Desquamative interstitial pneumonia (DIP)
Nonspecific interstitial pneumonia (NSIP)
Respiratory bronchiolitis-associated ILD (RB-ILD)
Lymphoid interstitial pneumonia (LIP)
What are the histologic hallmarks of hypersensitivity pneumonitis?
Airway-centered lymphocyte-predominant inflammation extending into alveolar septa
Loosely formed granulomas
What are the hallmarks of granulomatosis with polyangiitis?
Vasculitis - inflammation and invasion of blood vessels in the lung
c-ANCA positive cells
How can Langerhans cell histiocytosis be identified?
Multiple small bilateral lung nodules by CT
Stellate lesions with adjacent traction emphysema
Langerhans cells w/ prominent nuclear grooves, S-100 positive
Eosinophils
Birbeck granules by EM
What are some distinguishing features of cryptogenic organizing pneumonia (COP/BOOP)?
CT/CXR: Unilateral or bilateral consolidation, can have nodular opacities mimicking neoplasia
Histo: fibroblastic plugs within airspaces, variable inflammation of interstitium
How can acute interstitial pneumonia be identified?
Sudden onset - days-weeks
Ground glass opacities
Diffuse alveolar damage - hyaline membranes (acute/exudative phase) becoming loose organizing fibrosis in alveolar septa (organizing phase)
What are the defining features of desquamative interstitial pneumonia?
Mild interstitial fibrosis
Pigmented macrophages with light brown cytoplasmic pigment
More severe than RB-ILD
What is the DDx for wheezing?
B - bronchiolitis, bronchiectasis E - eosinophilic lung dz C - CHF A - asthma U - upper airway obstruction S - strongyloides (parasite) E - emboli O - obstructive lung dz F - foreign bodies G - GERD A - aspirin S - sinusitis
What is the DDx for bronchiectasis?
M - Marfan's syndrome U - ulcerative colitis C - CF O - obstructive lesions P - postpneumonic U - useless cilia (immotile cilia, Kartageners) S - sarcoid Y - Young's syndrome A - ABPA (allergic bronchopulmonary aspergillosis) I - Ig deficiency R - right middle lobe syndrome W - Williams-Campbell syndrome A - alpha-1-antitrypsin deficiency Y - Yellow Nail syndrome S - Swyer-James syndrome
What is the DDx for dysnpea/hypoxemia with normal CXR?
C - crazy (psychogenic) L - low hematocrit (anemia) E - emphysema A - asthma R - respiratory muscle weakness C - chest wall dz H - heart dz E - emboli S - sleep apnea T - tracheal dz S - shunt
What is the equation for O2 delivery or transport to tissues?
DO2 = CaO2 x CO DO2 = [1.34(Hb)(SaO2) + 0.003(PaO2)] x CO
What is type I respiratory failure and some common causes?
Hypoxemic respiratory failure - PaO2
What is type II respiratory failure and some common causes?
Hypercapnic respiratory failure - PaCO2 > 45mmHg
Incr. VD/VT, decr. resp. drive, decr. resp. pump, incr. WOB
Acute: Drug OD, spinal cord injury, acute NMD, COPD exacerbation, status asthmaticus
Chronic: chronic NMD, kyphoscoliosis, OHS, COPD
How does tx for acute hypoxemia differ from chronic?
Acute: shoot for PaO2 70-80mmHg, SpO2 > 95% w/ high flow O2, face mask with FiO2 > 50%
Chronic: only need PaO2 ~ 60mmHg, SpO2 90%; avoid worsening hypercapnia w/ low flow O2 therapy by nasal cannula/mask
What is the clinical definition of ARDS?
R - Respiratory failure (not CHF)
O - Onset (acute)
AC - Abnormal CXR - bilat. opacities, not explained by other processes
H - Hypoxemia (PaO2/FiO2
What is the approach to ARDS treatment?
Mech. ventilation - support while lungs recover
- lower tidal volumes protect the lung
- PEEP prevents atelectasis, improving PaO2
Supportive care - prophylaxis for ulcers, thromboembolism
Drug tx - abx if needed, NM blockade
What are four types of ventilator-induced lung injury?
Volutrauma - injury to lung indistinguishable from ARDS
Barotrauma - rupture of alveoli (PTX)
Biotrauma - cytokine-mediated injury secondary to initial lung injury
Atelectrauma - repetitive opening/closing of alveoli (prevented by PEEP)
What are the definitions of pre- and post-capillary pulmonary hypertension?
Pre-capillary: pulmonary arterial HTN, nl or reduced PCWP (15mmHg)
Post-capillary: pulmonary venous HTN, PCWP > 15mmHg
Pulm. HTN is defined as mean Pa >25mmHg
What is the WHO group I class of pulm HTN?
Pulmonary arterial HTN
Idiopathic & heritable
Assoc. w/ congen. heart dz, portopulmonary HTN, HIV, drugs, sickle cell
What is the WHO group II class of pulm HTN?
Pulmonary venous HTN
LV systolic dysfxn
Valvular defects - AS/MS
LV diastolic dysfxn - LV doesn’t relax, resulting in decreased preload and increased P
What is the WHO group III class of pulm HTN?
Pulm HTN w/ lung dz and/or chronic hypoxia Obstructive/COPD Restrictive/interstitial Hypoventilatory Sleep apnea High altitude
What is the WHO group IV class of pulm HTN?
Pulm embolic HTN
Chronic thromboembolic PH (CTEPH)
What is the WHO group V class of pulm HTN?
Misc. causes of PHTN
Sarcoid
Glycogen storage dz (Gaucher’s)
Hematologic, NF, tumor emboli, chronic renal failure
What is endothelin and what is its role in treating pulmonary HTN?
Molecule secr. by vascular endothelium and binds to smooth m. receptors, triggering contraction and eventual remodeling.
Tx: selectively block ETA receptor (more than ETB) - ETB binding triggers release of NO/PGI2 which cause vasodilation
What are some therapeutic measures than can be employed to treat pulmonary HTN?
General: Diuretics, digoxin, phlebotomy Anticoagulants Tx underlying dz (WHO groups II-V) Group I: vasodilators/anti-proliferative - Ca channel blockers - Prostacyclins - Endothelin receptor antagonists - PDE5 inh. -Guanylate cyclase stimulants
What are the three main risk factors for PE Dx?
Virchow’s triad:
- Stasis
- Inflammation
- Hypercoagulability
What histologic findings are consistent with pulmonary edema?
Pink transudate in alveolar spaces
Hemosiderin-laden macrophages (heart-failure cells)
Fibrotic thickening of alveolar septa (chronic edema)
What are three histologic hallmarks of severe, irreversible pulmonary HTN?
Plexiform lesion - vessels replaced by slit-like proliferative vascular spaces (resemble glomeruli)
Angiomatoid lesion - proliferation of thin-walled dilated and congested vessels
Necrotizing vasculitis - fibrinoid necrosis of intimal hyperplasia
