Respiratory Failure: Concepts and Sample MCQs (For NEET PG, USMLE, PLAB, FMGE /MCI Screening Entrance Exams) For more such notes and quizzes visit www.medicoapps.org

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Respiratory Failure: Concepts and Sample MCQs
(For NEET PG, USMLE, PLAB, FMGE /MCI Screening Entrance Exams)
Overview :
Respiratory failure isa syndrome in which the respiratory system failsin one or both of itsgasexchange functions: oxygenationand carbon
dioxide elimination. In practice, it may be classifiedaseither hypoxemic or hypercapnic.
Hypoxemic respiratory failure (type I) ischaracterizedby an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial
carbon dioxidetension(Pa CO2). Thisisthe most common form of respiratory failure,and it can be associatedwith virtually all acute diseases
of the lung, which generally involvefluidfilling or collapse of alveolar units. Some examplesof type I respiratory failure are cardiogenic or
noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
Hypercapnic respiratory failure (type II) ischaracterizedby a PaCO2 higher than 50 mm Hg. Hypoxemiaiscommonin patientswith
hypercapnic respiratory failure who are breathing room air. ThepH dependson the level of bicarbonate, which, in turn,isdependenton t he
duration of hypercapnia.Common etiologiesincludedrug overdose, neuromuscular disease, chest wall abnormalities, and severe airway
disorders (eg, asthma and chronic obstructivepulmonary disease [COPD]).
Respiratory failure may be further classifiedaseither acute or chronic.Although acute respiratory failure ischaracterized by life-threatening
derangementsin arterial bloodgasesand acid-base status, the manifestationsof chronic respiratory failure are lessdramatic andmay not be
as readily apparent.
Acute hypercapnic respiratory failure developsover minutesto hours; therefore, pH isless than 7.3. Chronic respiratory failure developsover
several days or longer, allowingtime for renal compensationand an increase in bicarbonate concentration. Therefore, thepH usually isonly
slightly decreased.
The distinction betweenacuteand chronic hypoxemic respiratory failure cannotreadily be madeon the basisof arterial blood gases. The
clinical markersof chronic hypoxemia, such aspolycythemiaor cor pulmonale, suggest a long-standing disorder.
Arterial blood gasesshould be evaluated inall patientswho are seriously ill or in whom respiratory failure issuspected. Ch est radiography is
essential. Echocardiography isnot routine butissometimesuseful. Pulmonary functionstests (PFTs) may be help ful. Electrocardiography
(ECG) should be performed to assess the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmiasresulting
from severe hypoxemia or acidosis. Right-sided heart catheterizationiscontroversial (see Workup).
Hypoxemia isthe major immediatethreat to organfunction. After the patient’shypoxemia iscorrected and theventilatory and hemodynamic
status have stabilized,every attempt shouldbe made to identify and correct the underlying pathophysiologic processthat led to respiratory
failure in the first place. The specific treatment dependson the etiology of respiratory failure (see Treatment).
For patient education resources, see the Lung and Airway Center, aswell asAcute Respiratory Distress Syndrome.
Pathology :
Respiratory failure can arise from an abnormality inany of the componentsof the respiratory system, including theairways, alveoli, central
nervoussystem (CNS), peripheral nervoussystem, respiratory muscles, and chest wall. Patientswho have hypoperfusion secondary to
cardiogenic, hypovolemic, or septic shockoften present with respiratory failure.
Ventilatory capacity isthe maximal spontaneousventilationthat can be maintainedwithout development of respiratory muscle fatigue.
Ventilatory demandisthe spontaneousminute ventilation that resultsin a stable Pa CO2.
Normally, ventilatory capacity greatly exceedsventilatory demand. Respiratory failure may result from either a reduction in ventilatory
capacity or an increase in ventilatory demand (or both). Ventilatory capacity can bedecreased by a disease process involvingany of the
functional componentsof the respiratory system and itscontroller. Ventilatory demandisaugmentedby an increase in minute ventilation
and/or an increase in the workof breathing.
Respiratory physiology
The act of respiration engages3 processes:
 Transfer of oxygen across the alveolus
 Transport of oxygen to the tissues
 Removal of carbon dioxidefrom blood intothe alveolusand thenintothe environment
Respiratory failure may occur from malfunctioningof any of these processes. In order to understand the pathophysiologic basisof acute
respiratory failure, an understandingof pulmonary gasexchange isessential.
Gas exchange
Respiration primarily occursat the alveolar capillary unitsof the lungs, where exchange of oxygenand carbon dioxidebetween alveolar gas
and blood takesplace. After diffusinginto the blood, theoxygenmoleculesreversibly bind to thehemoglobin. Eachmolecule of hemoglobin
contains4 sites for combinationwith molecular oxygen; 1 g of hemoglobin combineswith a maximum of 1.36 mL of oxygen.

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The quantity of oxygencombinedwith hemoglobindependson the level of blood Pa O2. Thisrelationship, expressed asthe oxygen
hemoglobin dissociation curve, isnot linear but hasa sigmoid-shapedcurve with a steep slope between a Pa O2 of 10 and 50 mm Hg and a
flat portion above a Pa O2 of 70 mm Hg.
The carbon dioxideistransported in 3 main forms: (1) in simple solution, (2) asbicarbonate, and (3) combined withprotein of hemoglobinas
a carbamino compound.
During ideal gasexchange, blood flow and ventilationwouldperfectly match eachother, resultingin no alveolar-arterial oxygen tension (PO2)
gradient. However, evenin normal lungs, not all alveoli are ventilatedand perfused perfectly. For a given perfusion,some alveoli are
underventilated, while othersare overventilated.Similarly, for known alveolar ventilation,some unitsare underperfused, wh ileothersare
overperfused.
The optimally ventilatedalveoli that are not perfused well have a largeventilation-to-perfusionratio(V/Q) and are called high-V/Q units
(which act like dead space). Alveoli that are optimally perfused but not adequately ventilatedare calledlow-V/Q units(which act like a shunt).
Alveolar ventilation
At steady state, the rate of carbon dioxide productionby the tissuesis constant and equalsthe rate of carbon dioxideelimination by the lung.
Thisrelationisexpressed by the followingequation:
VA = K × VCO2/ Pa CO2
where K is a constant (0.863), VA is alveolar ventilation,and VCO2 iscarbon dioxideventilation. Thisrelation determineswhether the alveolar
ventilation isadequate for metabolic needsof the body.
The efficiency of lungsat carrying out of respirationcan be further evaluated by measuring the alveolar-arterial PO2 gradient. Thisdifference
is calculated by the following equation:
PA O2 = FI O2 × (PB – PH2 O) – PA CO2/R
where PA O2 is alveolar PO2, FI O2 is fractional concentration of oxygen ininspiredgas, PB is barometric pressure, PH2 O is water vapor
pressure at 37°C, PA CO2 is alveolar PCO2 (assumed to be equal to Pa CO2), and R is respiratory exchange ratio. R dependson oxygen
consumption andcarbon dioxide production.At rest, the ratio of VCO2 to oxygen ventilation(VO2) isapproximately 0.8.
Even normal lungshave some degree of V/Q mismatching and a small quantity of right-to-left shunt, with PA O2 slightly higher thanPa O2.
However, an increase in the alveolar-arterial PO2 gradient above 15-20mm Hg indicatespulmonary disease asthe cause of hypoxemia.
Hypoxemic respiratory failure
The pathophysiologic mechanismsthat account for the hypoxemiaobserved in a widevariety of diseasesare V/Q mismatch and sh unt.
These 2 mechanismslead to wideningof the alveolar-arterial PO2 gradient, which normally islessthan 15 mm Hg. They can be differentiated
by assessing the response to oxygen supplementation or calculating theshunt fractionafter inhalationof 100% oxygen. In most patientswith
hypoxemic respiratory failure, these 2 mechanismscoexist.
V/Q mismatch
V/Q mismatch isthe most common cause of hypoxemia. Alveolar unitsmay vary from low-V/Q to high-V/Qin the presence of a disease
process. The low-V/Q unitscontribute to hypoxemiaand hypercapnia, whereasthe high-V/Q unitswaste ventilation but donot affectgas
exchange unlessthe abnormality isquite severe.
The low V/Q ratio may occur either from a decrease in ventilationsecondary to airway or interstitial lung disease or from overperfusion inthe
presence of normal ventilation. Theoverperfusion may occur in case of pulmonary embolism, where the blood isdivertedto normally
ventilated unitsfrom regionsof lungsthat have bloodflow obstructionsecondary to embolism.
Administrationof 100% oxygen eliminatesall of thelow-V/Q units, thusleadingto correction of hypoxemia. Hypoxemia increasesminute
ventilation by chemoreceptor stimulation,but the Pa CO2 generally isnot affected.
Shunt
Shunt isdefined asthe persistence of hypoxemia despite 100%oxygeninhalation. The deoxygenated blood (mixed venousblood) bypasses
the ventilated alveoli andmixeswith oxygenatedbloodthat hasflowedthroughthe ventilatedalveoli,consequently leadingt o a reduction in
arterial blood content. Theshunt iscalculatedby the followingequation:
QS/QT = (CC O2 – Ca O2)/CC O2 – Cv O2)
where QS/QT is the shunt fraction, CC O2 is capillary oxygencontent (calculatedfrom ideal PA O2), Ca O2 is arterial oxygencontent (derived
from Pa O2 by using the oxygen dissociation curve), and Cv O2 ismixed venousoxygen content (assumed or measured by drawing mixed
venousblood from a pulmonary arterial catheter).
Anatomic shunt existsin normal lungsbecause of the bronchial andthebesian circulations, which account for 2-3% of shunt. A normal right-
to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductusarteriosus, or arteriovenousmalformation in thelung.
Shunt asa cause of hypoxemia isobserved primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or
noncardiac origin. Hypercapnia generally doesnot developunlessthe shunt is excessive (> 60%). Compared with V/Q mismatch, hypoxemia
produced by shunt isdifficult to correct by meansof oxygen administration.

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Hypercapnic respiratory failure
At a constant rate of carbon dioxideproduction, Pa CO2 isdetermined by the level of alveolar ventilation according to the following equation
(a restatement of the equationgivenabovefor alveolar ventilation):
Pa CO2 = VCO2 × K/VA
where K is a constant (0.863). The relation betweenPa CO2 and alveolar ventilationishyperbolic. Asventilation decreasesbelow 4-6 L/min,
Pa CO2 rises precipitously. A decrease in alveolar ventilationcan result from a reductionin overall (minute) ventilationor an increase in the
proportion of deadspace ventilation.A reduction inminuteventilation isobserved primarily in the setting of neuromuscular disordersand
CNS depression. In pure hypercapnic respiratory failure, the hypoxemia iseasily corrected withoxygentherapy.
Hyperventilation isan uncommon cause of respiratory failure andusually occursfrom depression of the CNS from drugsor neuromuscular
diseases affecting respiratory muscles. Hypoventilation ischaracterizedby hypercapnia and hypoxemia.Hypoventilation can be
differentiated from other causesof hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.
Etiology
These diseases can be grouped according to theprimary abnormality andthe individual componentsof the respiratory system (eg, CNS,
peripheral nervoussystem, respiratory muscles, chest wall, airways, and alveoli).
A variety of pharmacologic, structural,and metabolic disordersof the CNS are characterized by depression of the neural driveto breathe.
Thismay lead to acute or chronic hypoventilation andhypercapnia.Examplesinclude tumorsor vascular abnormalitiesinvolving thebrain
stem, an overdose of a narcotic or sedative, and metabolic disorderssuch as myxedema or chronic metabolic alkalosis.
Disorders of the peripheral nervoussystem, respiratory muscles, and chest wall lead to an inability to maintain a level of m inuteventilation
appropriate for the rate of carbondioxide production. Concomitant hypoxemiaand hypercapnia occur. ExamplesincludeGuillain-Barré
syndrome, muscular dystrophy, myasthenia gravis, severe kyphoscoliosis, and morbid obesity.
Severe airway obstruction isa common cause of acuteand chronic hypercapnia. Examplesof upper-airway disordersare acute epiglottitis
and tumorsinvolving thetrachea;lower-airway disordersinclude COPD, asthma, and cystic fibrosis.
Diseases of the alveoli are characterizedby diffuse alveolar filling, frequently resultingin hypoxemic respiratory failure,althoughhypercapnia
may complicate theclinical picture. Common examplesare cardiogenic andnoncardiogenic pulmonary edema,aspiration pneumonia , or
extensive pulmonary hemorrhage. These disordersare associated with intrapulmonary shunt and an increased workof breathing.
Common causesof type I (hypoxemic) respiratory failure includethe following:
 COPD
 Pneumonia
 Pulmonary edema
 Pulmonary fibrosis
 Asthma
 Pneumothorax
 Pulmonary embolism
 Pulmonary arterial hypertension
 Pneumoconiosis
 Granulomatouslung diseases
 Cyanotic congenital heart disease
 Bronchiectasis
 Acute respiratory distress syndrome (ARDS)
 Fat embolism syndrome
 Kyphoscoliosis
 Obesity
Common causesof type II (hypercapnic) respiratory failure includethe following:
 COPD
 Severe asthma
 Drug overdose
 Poisonings
 Myasthenia gravis
 Polyneuropathy
 Poliomyelitis

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 Primary muscle disorders
 Porphyria
 Cervical cordotomy
 Head and cervical cord injury
 Primary alveolar hypoventilation
 Obesity-hypoventilation syndrome
 Pulmonary edema
 ARDS
 Myxedema
 Tetanus
Acute respiratory failure is defined as hypoxemia, which i.e; P aO 2 of <50mmHg. T his type of respiratory failure also consists of
marked V /Q abnormalities and shunting occurring within a lung.
Classification :
Type 1 respiratory failure occurs in the following clinical settings;
 A cute respiratory distress syndrome
 Fat embolism
 P ulmonary edema
Type 2 respiratory failure is a ventillatory failure having V /Q imbalance and inadequate alveolar ventilation. P atients with type 2
respiratory failures are divided in to categories, namely
 P atients with inherent lung disease (ex; include cystic fibrosis, emphysema, etc.)
 P atients with normal inherent lungs, but having inadequate ventilation (ex; include CNS disease, drug overdose and trauma.
Type 1 Respiratory Failure Type 2 Respiratory Failure Type 3 Respiratory Failure
O xygenation Failure
e.g. V /Q mismatch / shunt
V entilation Failure
e.g hypoventilation
Respiratory or C ombined Failure
e.g. combination
Low P O 2 Low P O 2 Low P O 2
Normal / Elevated PCO2 Elevated P CO2 Elevated P CO2
Elevated A -a Gradient Normal A -a Gradient Elevated A -a Gradient
1.
Whichof the followingstatementsare true about Flail chest?
1. Fracture of 3 or 4th ribs
2. Mechanical ventilationalways needed
3. Mediastinal shift
4. Inward movementof chestwall during inspiration
5. Ultimatelyleadsto Respiratory failure
 a.3,4,5 True & 1,2 False
 b. 3,4,5 False & 1,2 True

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 c.1,4,5 True & 2,3 False
 d.1,2,4 False & 3,5 True
 Fracture of 3 or 4th ribs andinwardmovementof chestwall duringinspirationare seeninFlail
chest.It will ultimatelyleadstorespiratoryfailure.
2.
Whichof the followingisa false statement about Type I respiratory failure:
 a.DecreasedPa02
 b.DecreasedPaC02
 c.Normal PaC02
 d.Normal A-agradient
 A-aGradientisthe difference betweenthe AlveolarPO2(A) andarterial PO2 (a).The a-a
gradientindicateshowwell O2isequilibratingacrossthe bloodairbarrier.
Acute respiratoryfailure isdefinedasalungdisorder,whereinadequate functioningof lung,to
meetthe necessarydemandsof anindividual isnotmet.Itisunable to maintainnormal levelsof
arterial gas inthe blood.Respiratoryfailure isof 3 types,namely
Type 1 respiratoryfailure orOxygenationFailure
Type 2 respiratoryfailure orVentilationFailure
Type 3 respiratoryfailure orCombinedRespiratoryFailure
3.
All of the followingagentscause respiratory failure due to central inhibitionofrespiratory centre,
EXCEPT:
 a.Opium
 b.Strychnine
 c.Barbiturate
 d.Gelsemium
 Strychnine:
It competitivelyantagonizesglycine,aninhibitoryneurotransmitterreleasedbypostsynaptic
inhibitoryneuronsinthe spinal cord.
It alsobindsto the chloride ionchannel,causingincreasedneuronal excitabilityandexaggerated
reflex arcs.

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Thisresultsingeneralizedseizure-like contractionof skeletalmuscles.
Deathusuallyiscausedbyrespiratoryarrestthat resultsfromintense contractionof the
respiratorymuscles.
4.
PneumatocelesinchestX-ray inan infantwith breathlesness,tachycardia, feverand respiratory
failure suggestsa diagnosisof:
 a. S.aureus
 b.Klebsiella
 c. Pneumothorax
 d. Airembolism
 RespiratorytractinfectionscausedbyS.aureus
A) In children,itcancause seriousrespiratorytractinfectionsinnewbornsandinfants;these
infectionspresentasshortnessof breath,fever,andrespiratoryfailure.Chestx-raymayreveal
pneumatoceles(shaggy,thin-walledcavities).
B) Inadults,nosocomial S.aureuspulmonaryinfectionsare commonlyseeninintubated
patientsinintensive care units.Patientsproduce increasedvolumesof purulentsputumand
developrespiratorydistress,fever,andnew pulmonaryinfiltrates.Distinguishingbacterial
pneumoniafromrespiratoryfailureof othercausesornew pulmonaryinfiltratesincriticallyill
patientsisoftendifficultandreliesonaconstellationof clinical,radiologic,andlaboratory
findings.
MUST KNOW:
Community-acquiredrespiratorytractinfectionsdue toS.aureususuallyfollow viral
infections—mostcommonlyinfluenza.Patientsmaypresentwithfever,bloodysputum
production,andmidlung-fieldpneumatocelesormultiple,patchypulmonaryinfiltrates.
5.
The antibioticwhich can cause respiratory failure whenused in patientswith myastheniagravis is:
 a.Telithromycin
 b.Clindamycin
 c.Linezolid
 d.Tetracycline
 Telithromycinmayleadtorespiratoryfailure.

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6.
Most common contributory factor to respiratory failure inpatients withcystic fibrosisis:
 a.H.Influenzae infection
 b.Pseudomonainfection
 c.Associatedheartfailure
 d.Hypokalemia
 P. aeruginosaisthe mostcommoncause of gram-negativebacteremiainneutropenicpatients
and itis the mostcommon contributingfactortorespiratoryfailure incysticfibrosisandis
responsible forthe majorityof deathsamongthem.P.aeruginosainfectioninburnsisnolonger
a major problem.