ICS_RESP_MSII

ABG -- ARTERIAL BLOOD GAS

• pH: 7.4
• -- <ACIDEMIC
• -- >ALKALEMIC

• PaO2: 90mmHg
• USED TO DETECT HYPOXEMIA
• DECREASES WITH AGING (75mmHg BY AGE 90). <=56-60 SIG HYPOXIA

• PaCO2: 40mmHg
• REFLECTION OF ACID/BASE BALANCE.
• HYPERCAPNIA >=45-50mmHg

CHANGE IN VOLUME DIVIDED BY CHANGE IN PRESSURE

MEASURE OF EASE AT WHICH LUNGS EXPAND

• REDUCED:
• PULM FIBROSIS
• PULM EDEMA
• ARDS

• INCREASED:
• EMPHYSEMA

CaO2 = (1.36 x Hgb x SaO2) + (0.003 x PaO2)

SaO2 IS SATURATION ... FRACTION OF BOUND Hg

CaO2 DEPENDS PRIMARILY ON Hg CONC AND O2 SAT OF ARTERIAL BLOOD, NOT THE ARTERIAL PARTIAL PRESSURE OF O2

R = 8 N L / pi r^4

• N = VISC
• L = LENGTH

RESISTANCE = PRESSURE DIFF / FLOW

• TURBULENT FLOW:
• --HIGH FLOW
• --HIGH GAS DENSITY
• --LARGE RADIUS
• --ONE OF ABOVE OR ALL 3

--25-40% IN UPPER AIRWAYS; GREATEST IN MEDIUM-SIZED BRONCHI

• LAMINAR:
• --ONLY IN SMALLEST AIRWAYS

• INCREASED RES:
• --ASTHMA
• --COPD
• --EMPHYSEMA
• --CHRONIC BRONCH

• NORM RES:
• --ARDS
• --ILD (INTERSTITIAL LUNG DISEASE)
• --PNEU

OXY TOXICITY -- DIFFUSE ALVEO DAMAGE PATTERN IN LUNG = ARDS

ABSORPTIVE ATELECTASIS (LACK OF NITROGEN IN ALVEO GAS ALLOWS OXY TO BE ABS AND ALVEO TO COLLAPSE

ASTHMA

COPD (EMPHYSEMA & CHRON BRONCHITIS)

• NORMAL RESISTANCE:
• --ARDS
• --ILD
• --PNEUMO

VENT = TIDAL VOL (TV) x RESP RATE IN 1 MIN

NORM PaCO2 = 40 torr

PAO2 = FiO2 (Pb_atm - P_H2O) - (Pa_CO2 / R)

• SIMPLIFIED STANDARD: sea level breathing room air
• --FiO2 = .21
• --Pb_atm = 760mmHg
• --Pb_H2O = 47mmHg
• --PaCO2 = 40
• --R = 0.8

PAO2 = 150 - (PaCO2 / 0.8)

EFFICIENCY OF LUNG

PAO2 - PaO2

NORMAL IS 3-16 mmHg

VARRIES ACCORDING TO AGE

• ELEVATED:
• --V/Q MISMATCH
• --RIGHT/LEFT SHUNTS
• --IMPAIRED DIFFUSION

• NORMAL:
• --HIGH ALTITUDE
• --ALVEO HYPOVENT

VOL GAS REMAINING IN THE LUNGS AT END OF NORMAL TIDAL EXPIRATION

RV + ERV

IC = MAX VOL GAS INHALED AFTER NORMAL TIDAL EXHALE

TLC = VOL GAS INHALED AFTER MAX EXHALE (INCLUDING RV)

VC = (TLC - RV)

AGE, SEX, HEIGHT, ETHNICITY

FVC >= 80%

FEV1 >=80%

FEV1/FVC >= 70-75%

TLC 80-120%

RV 80-120%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

FVC >= 80%

FEV1 >=80%

FEV1/FVC >= 70-75%

TLC 80-120%

RV 80-120%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

FVC >= 80%

FEV1 >=80%

FEV1/FVC >= 70-75%

TLC 80-120%

RV 80-120%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

FVC >= 80%

FEV1 >=80%

FEV1/FVC >= 70-75%

TLC 80-120%

RV 80-120%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

FVC >= 80%

FEV1 >=80%

FEV1/FVC >= 70-75%

TLC 80-120%

RV 80-120%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

• DLCO (DIFFUSION CAPACITY IN L OF CO)
• 80-100%

• CAUSES:
• --THICKENING OF ALVEO-CAPIL MEM (PULM FIBROSIS, ILD, INTERSTITIAL OR ALVEO EDEMA)

--DEC SURFACE AREA (EMPHYSEMA, TUMORS, LOW PULM CAPIL BLD VOL

--DEC ERYTH UPTAKE (ANEMIA)

--V/Q MISMATCH

IMLPY REDUCED ABILITY TO GET AIR THROUGH COND AIRWAYS AND OUT LUNGS

FEV1/FVC RATION < 75% (COPD AT <70%)

• DISEASES:
• --COPD (EMPH & BRONCHITIS)

--BRONCHIECTASIS (POST INF AND CYCSTIC FIBROSIS)

--ASTHMA

OFTEN ASTHMA & COPD WILL SHOW HYPERINFLATION (TLC > 120%) AND AIR TRAPPING (RV > 120%)

• RESTICTIVE:
• --PULM FIBROSIS
• --ILD
• --INFILT LUNG DISEASE ( MALIG LYMPH SPREAD)
• --PLEURAL DISEASE
• --NEUROMUSC
• --OBESITY
• --CHEST WALL DEFORMITIES (KYPHOSIS, PECTUS EXCAVATUM)

BLEOMYCIN -- CHEMO DRUG --> PRE-OP TO 100% SAT CAUSING OXYGEN RADIACALS

AMIODARONE -- CARDIAC AGENT

METHOTREXATE -- IMMUNOSUPPRESSANT

CRACK/COCAINE

INABILITY TO GET AIR INTO LUNGS AND MAINTAIN NORMAL LUNG VOL

AIR FLOW NOT AFFECTED

--DEC TLV <80% PREDICTED. GOLD STANDARD

--LOW FVC <80%

--NORMAL FEV1/FVC RATIO IS SUGGESTIVE OF RESTRICTIVE PHYS, BUT MUST CONF BY GETTING LUNG VOLS (TLC)

--CANNOT Dx WITH SPIROMETRY ALONE

• DISEASES:
• --PULM FIBROSIS
• --ILD
• --INFILTRATIVE LUNG DISEASE (MALIG SPREAD THRU LYMPH)
• --PLEURAL DISEASE
• --NEUROMUSC DISEASE
• --OBESITY
• --CHEST WALL DEFORMITIES (KYPHOSIS, PECTUS EXCAVATUM)

LOW FEV1 or FVC = OBST or REST

LOW FEV1/FVC = OBST

nL FEV1/FVC w LOW TLC = REST

----------------------------------------

nL FVC & FEV1 >= 80%

nL FEV1/FVC >= 75%

nL TLC & RV >80% & < 120%

INABILITY TO MAINTAIN EITHER NORM DELIVERY OF OXY OR NORM REMOVAL OF CO2

• CAUSES:
• --HYPOXEMIA (PaO2 <= 50-60mmHg)
• --HYPERCAPNIA (PaCO2 >= 45-50mmHg)

• OFTEN PATIENS IN "50/50 CLUB"
• --HYPOXIMIA (PaO2 <= 50-60mmHg)
• --HYPERCAPNIA

P/F RATION

PaO2/FiO2

USED IN Pt WITH SUPP OXY

nL RATIO ~ 500 (100mmHg/0.21

ACUTE LUNG INJURY ALI = P/F <= 300

ARDS <= 200

• ACUTE LUNG INJURY (ALI)
• --NON-CARDIOGENIC PULM EDEMA WITH PaO2/FiO2 <= 300mmHg

ARDS <= 200mmHg

EXTREME V/Q MISMATCH

• DEAD SPACE VENTILATION, NO PERFUSION
• --MASSIVE PULM EMBOLISM
• --CARDIAC SHUNTS

ONLY CAUSE OF HYPOXEMIA NOT CORRECTED WITH SUPP O2

SUPPORTIVE

--1st "THE ABCs" AIRWAY, BREATHING, CIRC

--THEN SPECIFIC TREATMENTS DIRECTED AT UNDERLYING DESEASE. GENERALLY, PaO2 ~ 60mmHg USUALLY CORRESPONDING TO SaO2 ~ 90% IS ADEQUATE TARGET

CLINICAL CLASSIFICATION BASED ON CHEST X-RAY -- WHITE OR BLACK

• WHITE:
• --PNEUMONIA
• --ARDS
• --CARDIOGENIC PULM EDEMA: CHF
• --ILD

• BLACK:
• --OBST LUNG DISEASE
• --PULM EMBOLI
• --PLEURITIC PAIN, HEMOPTYSIS, RISK FACTORS OF DVT
• --MICRO ATELECTASIS
• --SHUNT

--WHITE CXR

--INFILTRATES WITH SUPP CLINICAL FEATURES (FEVER, LEUKOCYTES, SPUTUM PROD)

--ELDERLY Pt OVER 65 LACK PULM SYMP 50% OF TIME AND MANY PRESENT w CONF AND LETHARGY & FATIGUE

--WHITE CXR

--NON-CARDIOGENIC PULM EDEMA

• --MOST Pt WITH ARDS HAVE ONE OF THE COMMON PRECIP FACTORES LEADING TO DISORDER
• ----SEPSIS
• ----HYPOTEMSION
• ----MASSIVE TRAUMA
• ----TRANSUFIONS

• LESS COMMON:
• --PANCREATITIS
• --DRUG OVERDOSE
• --POST CARDIO-PULM BYPASS SURGERY

--WHITE CXR

--PULM CAPILL WEDGE PRESSURE >18mmHg

--USUALLY IN SETTING OF MYOCARDIAL INFARCT, SEVERE HYPERTENSION, VALVE DISEASE

--WHITE CXR (DOTS AND LINES OR RETICULONODULAR PATTERN)

--USUALLY SLOWLY PROG DISEASE

--HIST AND OLD CXR VERY HELPFUL

--BLACK CXR

--BEDSIDE SPIROMETRY (FEV1/FVC <75%) VERY HELPFUL

--OFTEN w WHEEZING, PROLONGED EXPIRATION (1:3 OR 1:4) AND DEC BREATH SOUNDS ON PHYSICAL EXAM

--BLACK CXR

--MAY HAVE SIG HYPOX WITH nL CXR

--MOST PRESENT w ACUTE DYSPNEA

--PLEURITIC PAIN, HYMOPTYSIS, OR RISK FACTORS OF DVT INC LIKELYHOOD

--BLACK CXR

--POST-OP Pt OR Pt WHO BREATH SHALLOW FROM PLEURITIC PAIN (RIB FRAC)

--BLACK CXR

--PULM ARTERIAL-VENOUS MALFORMATIONS (AVM) OR MICRO AVMs IN CIRRHOSIS (SPIDER ANGIOMAS OR LUNG)

--INTRACARDIAC: Rt TO Lt SHUNTS FROM CONG OR ACQ HRT DISEASE AND/OR PULM HYPERTENSION. Dx BY BUBBLE ECHOCARDIOGRAM

Level of diaphragm rises 4 cm

Diaphragmatic excursion increases

Subcostal angle increases

Transverse diameter of chest increases 2 cm

• Chest circumference increases 6 cm
• --------------------------------------

ELEV OF DIAPHRAGM WITH INC UTERINE SIZE. MAKES RESP PRIM THORASIC AND MINIMALLY ABDOMINAL

SUBCOSTAL ANGLE INC MAKES RESP MOVEMENTS SHALLOWER

• VITAL CAPACITY
• --PROB SMALL INC (100-200ml)
• --INSP CAP MAY INC BY 300ml
• --EXP RESERVE VOL DEC BY 200ml
• --RV/FUNC RESID CAP DEC BY 20%

• TIDAL VOLUME:
• --INC BY 40% (500 --> 700ml)
• --RESP RATE NOT CHANGED
• --MIN VENT RISES IN PARALLEL TO INC TIDAL VOL BY 40%

PREG WOMAN INC VENT BY BREATHING MORE DEEPLY, BUT NOT MORE FREQUENTLY

VENT CHANGE PRIM BY CENTRAL RESP CONTROL

INC VENT IN PREG PROVIDES SOME INC OXY, BUT REALLY REMOVES CO2

-->DROP IN pCO2

--PROGESTERONE LOWERS THRESH OF RESP CENTER TO pCO2 AND IS THE MECH OF HYPERVENT AND WASH-OUT.

SMALL pO2 CHANGE bc OF SHAPE OF Hg DISSOCIATION CURVE; THERE IS LITTLE INC IN Hg SAT

FALL IN pCO2 IS MATCHED BY AN EQUIV FALL IN PLASMA BICARB AND NO CHANGE IN ART pH. LOSS OF BICARB MAKES PREG MORE SUSCEPTIBLE TO ACIDOSIS (LESS BUFFERING)

VENOUS pH BECOMES SLIGHTLY MORE ALKALOTIC (7.35 --> 7.38)

pH______ 7.4 / 7.42

PaO2___ 100 / 100

PaCO2__ 35-40 / 30

BICARB_ 24 / 20

• PHYSICAL:
• immature

less surface area for gas exchange,

capillaries far from those units,

presence and maturity of surfactant

FLUID REABSORPTION -- NEEDED FOR GAS EXCHANGE

LOW PVR; HIGH SVR

INC O2 CAUSES VASODILATION IN PULM ARTERIOLES BY enhancement of prod of endothelium-derived vasodilators PROSTOGLANDIN I2 (prostacyclin) and NO.

• FORAMEN OVALE; DUCTUS ARTERIOSUS

SUSTAINED BREATING -- CNS

•In utero, lungs are chloride secreting. During the last weeks of a normal pregnancy and during onset of labor, hormonal changes facilitate reabsorption of fluid. “Vaginal squeeze” of minimal importance.

•Rapid fluid clearance mediated by transepithelial sodium reabsorption through amiloride-sensitive sodium channels in alveolar epithelial cells.

•Must go via lymphatics to venous system.

•Failure of clearance quite common, esp. in elective c-section, prematures.

•Retained fetal lung fluid causes Transient Tachypnea of the Newborn (TTN), exacerbates RDS, pneumonia.

•POSSIBLE SURFACTANT DEFICIENCY

•DECREASED DRIVE TO BREATHE

•RAPID HEAT LOSS, POOR TEMPERATURE CONTROL

•POSSIBLE INFECTION

•SUSCEPTIBLE TO BRAIN HEMORRHAGE

•SUSCEPTIBLE TO HYPOVOLEMIA SECONDARY TO BLOOD LOSS

•WEAK MUSCLES MAKE SPONTANEOUS BREATHING DIFFICULT

• •IMMATURE TISSUES MAY BE DAMAGED BY
• EXCESSIVE OXYGEN

•HETEROGENEOUS MIXTURE OF PHOSPHOLIPIDS AND PROTEINS SECRETED BY TYPE II PNEUMOCYTES

•PRESENT IN SECRETORY ORGANELLES AT 24 WEEKS

• •SURFACTANT LIPIDS NOT DETECTABLE IN
• AMNIOTIC FLUID UNTIL AROUND 30 WEEKS

•MAJOR COMPONENTS - DPPC, PG, APOPROTEINS (SP-A, SP-B, SP-C, SP-D)

• •EXOGENOUS SURFACTANT AVAILABLE AS
• TREATMENT; GIVEN VIA ENDOTRACHEAL TUBE

• SYMPTOMS
• --STRIDOR,
• --SNORING,
• --APNEA,
• --HOARSENESS,
• --BRASSY COUGH

• COURSE
• --ACUTE
• --RECURRENT
• --CHRONIC
• --PROGRESSIVE

• EXAM
• --INSPIRATORY = STRIDOR- SUPRAGLOTTIC

--EXPIRATORY = STRIDOR- LOWER TRACHEA

--BIPHASIC = GLOTTIC OR SUBGLOTTIC

--VOICE CHANGES = LARYNGEAL

--MOST COMMON CAUSE OF NONINFECTIOUS, RECURRENT OR PERSISTENT STRIDOR IN INFANTS

--PRESENTS FIRST 6 WKS LIFE. IMPROVES WITH AGE, RESOLVES BY 1- 2YRS.

• --COLLAPSE OF SUPRAGLOTTIC STRUCTURES (ARYTENOID CARTILAGE AND EPIGLOTTIS) DURING INSPIRATION
• -------------------------

• CLINICAL
• --WORSE
• IN SUPINE, WITH INCREASED ACTIVITY, CRYING , URI, FEEDINGS, +/- GERD

--CLINICAL DIAGNOSIS – SUPPORTIVE MEASURES AND REASSURANCE, RARELY LIFE THREATENING.

--IMAGING - ONLY IF FEEDING ISSUES, SEVERE STRIDOR, SLEEP APNEA, DYSPNEA, FTT

VIRAL CROUP-LARYNGOTRACHEOBRONCHITIS: EDEMA IN THE SUBGLOTTIC SPACE, INFLAMMATION OF ENTIRE AIRWAY.

• EPIDEMIOLOGY-
• --6MONTHS- 3 YEARS
• --MALES 2X > FEMALES
• --FALL & WINTER (OCT-MAY)
• --PARAINFLUENZA TYPE 1,2,3,
• --RSV, ANDENOVIRUS, INFLUENZA,
• --MYCOPLASMA (ESP > 5 YR),
• --RUBEOLA.

•CLINICAL PRESENTATION

• –SYMPTOMS: RHINORRHEA, CORYZA,
• COUGH, IRRITABILITY, POOR FEEDING, EMESIS

• –EXAM:
• •TACHYPNEA, WHEEZING, LABORED
• RESPIRATIONS, USE OF ACCESSORY MUSCLES, AND/OR NASAL FLARING, HYPOXIA, WHEEZES / CRACKLES ON EXAM

• •CXR- HYPERINFLATION, SUBSEGMETAL
• ATELECTASIS, PERIHILAR STREAKING

–COURSE- 2-4 WEEKS

• –1/3 INFANTS WILL HAVE RECURRENT
• WHEEZING

• –TREATMENT LARGELY SUPPORTIVE-
• OXYGEN, CLEARING SECRETIONS, SUPPORT OF HYDRATION/NUTRITION.

–PREVENTION- IMMUNOPROPHYLAXIS FOR HIGH RISK INFANTS

• --------------------------------------
• VIRAL INFECTION OF THE LRT

•EPIDEMIOLOGY

• –MOST COMMON SERIOUS ACUTE
• RESPIRATORY ILLNESS IN INFANTS/CHILDREN UNDER 2YRS.

• •NINETY PERCENT OF CHILDREN ARE
• INFECTED WITH RSV IN THE FIRST 2 YEARS OF LIFE

• •INFECTION WITH RSV DOES NOT GRANT
• PERMANENT OR LONG TERM IMMUNITY. REINFECTIONS ARE COMMON AND MAY BE EXPERIENCED THROUGHOUT LIFE

• –WINTER /EARLY SPRING
• (DECEMBER-MARCH)

• –RSV, ADENOVIRUS, PARAINFLUENZA,
• INFLUENZA, PNEUMOVIRUS, HUMAN METAPNEUMOVIRUS

•PATHOGENESIS

–CONTACT AND DROPLET DISPERSION

CHARACTERIZED BY ACUTE INFLAM, EDEMA AND NECROSIS OF EPITHELIAL CELLS LINING SMALL AIRWAYS, AND INCREASED MUCUS PRODUCTION.

•NOT ALL WHEEZY BABIES HAVE ASTHMA OR GO ON TO BE WHEEZY ADULTS!

•BRONCHIOLITIS = COMMON VIRAL LRTI

•BRONCHOCONSTRICTION INC MUCUS PRODUCTION = SMALLER AIRWAY CALIBER

•INCREASED CHEST WALL COMPLIANCE AND INCREASED ELASTIC RECOIL → DECREASED RESIDUAL VOLUME (SO MORE QUICKLY SYMPTOMATIC)

• •DIFFERENTIAL DIAGNOSIS: CONGENITAL
• ANOMALIES/MALFORMATION OF THE AIRWAYS, CF, GER, IMMUNE DEFECT

•$$$ IMPLICATIONS

• CYSTIC FIBROSIS TRANSMEMBRANE
• CONDUCTANCE REGULATOR (CFTR)

LOCATED IN SWEAT GLANDS, RESPIRATORY EPITHELIUM, PANCREAS, INTESTINE, LIVER, REPRODUCTIVE TRACT

MEMBRANE SPANNING CHANNEL THAT CONTROLS CHLORIDE MOVEMENT

CHROMOSOME 7

–>1000 KNOWN MUTATIONS

–DF508-MOST COMMON MUTATION

–MODIFIER GENES PLAY A ROLE