a c u t e r e s p i r a t o r y f a i l u r e

ACUTE RESPIRATORY FAILUREACUTE RESPIRATORY FAILURE

• EMERGENCY CONDITION

• ALL AGES

• MAJOR CAUSE OF DEATH

• SUCCESSFUL OUTCOME DEPENDS ON PROMPT RECOGNITION AND IMMEDIATE INITIATION OF SUPPORTIVE Rx

ARF-DEFINITIONARF-DEFINITION (Campbell 1960-BRMEDJ. 19651:1451)(Campbell 1960-BRMEDJ. 19651:1451)

• 10 FUNCTION FAILURE OF O2 AND CO2 EXCHANGE

• Pa O2 <60 Mm Hg OR Pa CO2 >50,WHILE BREATHING AIR @ SEA LEVEL

ARF-CAUSESARF-CAUSES

• ACUTE PULMONARY PROBLEMS

• BUT ALSO IN PATIENTS WITH NORMAL LUNGS:– SHOCK– MYOCARDIAL INFARCTION– BURNS

CAUSESCAUSES

• PUMP• Respiratory center• Peripheral nerves• Respiratory muscles• Chest wall• Lungs• Parenchyma• Vasculature

NORMAL GAS EXCHANGENORMAL GAS EXCHANGE

• BRANCHING CAPILLARIES ALLOW THE DIFFUSION OF OXYGEN AND CARBON DIOXIDE BETWEEN THE ALVEOLI AND THE BLOOD

• OXYGEN IS REVERSIBLY BOUND TO HEMOGLOBIN

• 100 ML BLOOD NORMALLY CONTAINS 18 TO 20 ML OF OXYGEN

• CO2 +H2OH+ + HCO3

DECREASED MIXED VENOUS ODECREASED MIXED VENOUS O22 SATURATION (SvOSATURATION (SvO22))

• O2 RETURNING TO THE LUNGS FROM THE SYSTEMIC CIRCULATION

• SvO2 = SaO2 - [VO2/HgBx CO]

MIXED VENOUS DESATURATIONMIXED VENOUS DESATURATION

• LOW VALUES OF Hg (ANEMIA)

• LOW VALUES OF CO (CARDIAC OUTPUT)– eg. CARDIOGENIC SHOCK

DIFFUSIONDIFFUSION

• CO2 DIFFUSES ACROSS THE CAPILLARY MEMBRANE 20X FASTER THAN O2

• PCO2 IS A INDICATOR OF THE ADEQUACY OF VENTILATION

• PO2 CAN BE AFFECTED BY BOTH VENTILATION AND DIFFUSION

• ELEVATED PCO2=HYPOVENTILATION• DECREASED PCO2=HYPERVENTILATION

SHUNTSHUNT

• VENOUS - VENOUS BLOOD GOES TO THE SYSTEMIC CIRCULATION WITHOUT OXYGENATION

• ABNORMAL VASCULAR OR CARDIAC COMMUNICATIONS

• PERFUSING COMPLETELY UNVENTILATED LUNGS

– eg. FLOODED, CONSOLIDATED

• SHUNT IS REFRACTORY TO O2 RxSHUNT IS REFRACTORY TO O2 Rx

V/Q MISMATCHINGV/Q MISMATCHING

• USUALLY FROM NORMAL PERFUSION OF POORLY VENTILATED LUNGS

– BRONCHOSPASM

– EDEMA

– SECRETIONS

• HYPOXEMIC PULMONARY VASOCONSTRICTION IS FREQUENTLY IMPERFECT

• UNDERPERFUSION OF NORMALLY VENTILATED LUNGS IS LESS COMMON (P.E.)

• V/Q MISMATCHING RESPONDS TO SUPPLEMENTAL O2 AS EVEN POORLY VENTILATED LUNGS CAN GET O2 TO RBC’S

RESPIRATORY EXCHANGE RESPIRATORY EXCHANGE RATIORATIO

• FOR EACH 5 ML OF O2 CONSUMED 4 ML OF CO2 IS PRODUCED.

• 4/5 = 0.8

• WE CAN’T MEASURE pAO2 DIRECTLY.• we use the pCO2 and the respiratory

exchange ratio to estimate the alveolar pO2 ie pAO2

A-a O2 DIFFERENCEA-a O2 DIFFERENCE

• PAO2 = FIO2 X ( Pb – PHO2) – PACO2/R PAO2= MEAN ALVEOLAR O2• PHO2 = WATER VAPOR PRESSURE• Pb = BAROMETRIC PRESSURE• R = RESPIRATORY EXCHANGE RATIO= .8

• PAO2 = .21 X ( 760mm Hg - 47 mmHg ) - PaCO2/.8

• PAO2 = 150 mm Hg – PaCO2/.8

• P (A - a ) O2 = 150 – ( PaO2 + PaCO2/.8 )

A-a DIFFERENCEA-a DIFFERENCE

• [150 - (PaCO2/0.8] - PaO2

• WHEN A PATIENT IS ON SUPPLEMENTAL O2----- THE CALCULATION OF O2 CONCENTRATION IS IMPRECISE. THEREFORE, CALCULATION IS ONLY REALLY GOOD FOR ROOM AIR

• RULE OF 7: MULTIPLY F1O2 BY 7 GIVES ROUGH IDEA @ BEDSIDE OF WHAT THE PaO2 SHOULD BE– eg. 100% = 700– eg. 50% = 350

A-a O2 DIFFERENCEA-a O2 DIFFERENCE

• MOST SENSITIVE INDICATOR OF RESPIRATORY DISEASES THAT INTERFERE WITH GAS EXCHANGE

• HELPS TO DIFFERENTIATE PULMONARY FROM EXTRAPULMONARY CAUSES OF HYPOXIA AND HYPERCAPNIA

A-a GRADIENTA-a GRADIENT

• N < 15

• OLDER PERSONS– 2.5 +.25*AGE– eg. AGE 60, 2.5+15=17.5– eg. AGE 80, 2.5+20=22.5

RESPIRATORY FAILURERESPIRATORY FAILURE

• A BLOOD GAS DIAGNOSIS

• TWO MAJOR TYPES:

• I) HYPOXEMIC PaO2 <55-60

• II) HYPERCARBIC Pco2 >50

• not absolute values-consider the patient’s baseline: age,FIO2, clinical condition

HYPOXEMIC RESPIRATORY HYPOXEMIC RESPIRATORY FAILUREFAILURE

• HYPOVENTILATION-cns

• V/Q MISMATCH -most common

• SHUNT-anatomic-VSD,PDA, PFA; physiologic: pneumonia,atelectasis, pulmonary edema, ARDS

• DIFFUSION LIMITATION• REDUCTION IN FIO2

HYPOXEMIC RESPIRATORY FAILUREHYPOXEMIC RESPIRATORY FAILURE

• HEALTHY:– SMOKE INHALATION– CO POISONING– TRAVEL TO HIGHER ALTITUDE

• COPD– AIRPLANE RIDE (~6,000 TO 8,000 Ft) PaO2 (80 TO

100 DOWN TO 60 0R 70)

HYPOXEMIC RESPIRATORY FAILUREHYPOXEMIC RESPIRATORY FAILURE

• HYPOVENTILATION:– O2 CONSUMPTION > REPLACEMENT BY

VENTILATION

• ROOM AIR A-a GRADIENT– P[A-a]O2=[150-(Pa CO2/0.8)-Pa O2]– eg. 5=[150-40/0.8-95]

HYPOXEMIC OR HYPERCAPNEIC HYPOXEMIC OR HYPERCAPNEIC (HYPERCARBIC)(HYPERCARBIC)

• DECEASED PO2 VS. INCREASED PCO2• INCREASED P[A-a]O2 -ALVEOLAR-

ARTERIAL TENSION DIFFERENCE IS COMMON WITH NL OR DECREASED pCO2

IMPAIRED DIFFUSIONIMPAIRED DIFFUSION

• PROCESSES THAT INCREASE THE DISTANCE FROM ALVEOLI TO CAPILLARIES– eg. IPF

• PROCESSES THAT LOWER O2 DIFFUSION GRADIENT – eg. CO POISIONING– ABNL HG– ANEMIA

• IMPAIR DIFFUSION FROM ALVEOLI TO VENOUS BLOOD

HYPERCAPNEIC RESPIRATORY FAILUREHYPERCAPNEIC RESPIRATORY FAILURE

• IMBALANCE BETWEEN SUPPLY (STRENGTH) AND DEMAND (LOAD)

• CLUES:– UNEXPLAINED ALTERED NEURAL STATUS– HEADACHES– PAPILLEDEMA– TACHYCARDIA– HYPERTENSION– ELEVATED SERUM BICARBONATE LEVEL

HYPERCAPNEIC RESPIRATORY HYPERCAPNEIC RESPIRATORY FAILUREFAILURE

• 1) INSUFFICENT DRIVE: idiopathic, central sleep apnea, overdose, hypothyroidism

• 2) INCREASED VENTILATORY WORK LOAD: increased CO2 production (i.e. burns),increased dead space with wasted ventilation (e.g.massive PE ),disorders of the chest wall

HYPERCAPNEIC RESPIRATORY HYPERCAPNEIC RESPIRATORY FAILURE (cont)FAILURE (cont)

• Pump failure: motor neurons ( spinal cord injury,

tetanus, polio), peripheral neuropathy (Guillan Barre, polyneuropathy of critical illness)

• Neuromuscular junctions (myasthenia gravis,et al )

• Respiratory muscles (muscular dystrophy, et al.)

HYPERCAPNEA WITH O2 HYPERCAPNEA WITH O2 ADMINISTRATIONADMINISTRATION

• INCREASED V/Q MISMATCH

• LOSS OF HYPOXIC VENTILATORY DRIVE

• HALDANE EFFECT-O2 decreased CO2 bound to hemoglobin increasing PaCo2

• MUST BE CAREFUL WHEN ADMINISTERING O2 TO PATIENTS WITH COPD

HYPOXEMIC & HYPOCAPNEIC RESPIRATORY HYPOXEMIC & HYPOCAPNEIC RESPIRATORY FAILURE CAN OCCUR TOGETHERFAILURE CAN OCCUR TOGETHER

• PaCO2 + P(A - a)O2 ARE HIGH

• PaO2 LOW

• V/Q MISMATCH

• (REPIRATORY MUSCLE FATIGUE)

MAKING THE DXMAKING THE DX

• IDENTIFY HYPOXEMIC ARF

• IDENTIFY CAUSE:– ? NOT APPARENT, REVIEW Hx & FE– ? HEART DISEASE-CHF– COLLAGEN VASC.-ALVEOLAR

HEMORRHAGES– NON INFECTION PN– MALIGIANCY-LYMPHAMPITIC SPREAD

ABG IMPORTANTABG IMPORTANT

• WON’T BREATHE– INSUFFICIENT DRIVE

• CAN’T BREATHE– INSUFFICIENT STRENGTH:

• WEAKNESS• TOO HIGH WORKLOAD• BOTH

FACTORS AFFECTING ABGFACTORS AFFECTING ABG

• AGE• FIO2

• PREVIOUS MEDICAL CONDITION

• METABOLIC STATE

• PHYSICAL POSITION

• BAROMETRIC PRESSURE

RESPIRATORY FAILURE VS. RESPIRATORY FAILURE VS. RESPIRATORY INSUFFICIENCYRESPIRATORY INSUFFICIENCY

• FAILURE (ACUTE OR CHRONIC)– ABNL ABG’S

• INSUFFICIENCY– ABG’S MAY BE NL, BUT ABNL SIGNS &

SYMPTOMS USUALLY PRESENT• eg. DYSPNEA, PARADOXICAL BREATHING

ARF CAN PRESENTARF CAN PRESENT

• ALTERED MENTAL STATUS

• LETHARGY

• COMA

• UNEXPLAINED TACHYCARDIA

• ABG ANALYSIS IS IMPORTANT

EARLY RECOGNITION OF ARI EARLY RECOGNITION OF ARI CAN AVERT ARFCAN AVERT ARF

• DEVIATION OF RESPIRATORY RATE (BASELINE)

• TRAJECTORY OF DECLINE

• NATURAL HX OF MOST UNDERLYING PROCESS

ARF-APPROACHARF-APPROACH

• DETERMINE EXTENT OF SUPPORTIVE RX REQUIRED (O2 SUPPLEMENTATION, VENT)

• DX UNDERLYING DISORDERS (IF ANY)

– Hx, PE– BEGIN SPECIFIC CONCOMITANT RX

MANAGEMENTMANAGEMENT

• RECOGNIZE TYPE- hypercapneic, hypoxemic, both

• TREAT UNDERLYING ETIOLOGY – asthma, CHF, pneumonia

• OXYGEN – usually the most single useful treatment

INDICATIONS FOR INTUBATIONINDICATIONS FOR INTUBATION

• PERSISTENT HYPOXEMIA

• PROGRESSIVE ACIDEMIA

• PROGRESSIVE HYPERCAPNEA

• ALTERATION IN MENTAL STATUS

• EVIDENCE OF RESPIRATORY MUSCLE FATIGUE

• ETT 7.5 mm-ease of weaning, possible bronchoscopy

INITIAL VENT SETTINGSINITIAL VENT SETTINGS

• FIO2: 90-100

• Tidal Volume 8-10 ml/kg

• Mode IMV or AC 8-12 B/min.

• Peep: 0-5 cm water

INITIAL VENT MANAGEMENTINITIAL VENT MANAGEMENT

• Examine patient carefully and see how the patient tolerates ventilation

• Obtain chest xray to determine ETT position

• Obtain ABG 15- 20 mins and adjust ventilator accordingly

• Monitor blood pressure –?auto peep

KEY DECISIONKEY DECISION

• WHEN TO INTUBATE?

• AVOID WHEN POSSIBLE, BUT DON,T WAIT TOO LONG IF YOU ARE GOING TO DO IT

EXAMPLE OF USE OF A-a EXAMPLE OF USE OF A-a GRADIENT CALCULATIONGRADIENT CALCULATION

• HEROIN OVERDOSE– RA ABG 7.08– PaO2 40– PaCO2 80– 150-80/.8-40=10– THEREFORE, HYPOVENTILATION SOLE

CAUSE

CLINICAL MODES OF CLINICAL MODES OF VENTILATIONVENTILATION

• Controlled– Volume– Pressure

• Assisted– IMV– SIMV– Pressure Support

Assist/Control

TYPES OF VENTILATORSTYPES OF VENTILATORS

• A) Negative pressure– Cuirass– Tank

• B) Positive pressure– Pressure limited– Volume limited

• C) High frequency devices– Jet– High frequency– Oscillators

POSITIVE PRESSURE POSITIVE PRESSURE VENTILATORS VENTILATORS

• Classification is based on the Mechanism of termination of inspiration:– Pressure– Volume– Time– Flow (few)

MECHANICAL VENTILATIONMECHANICAL VENTILATION

• 1) Triggering mechanism

• 2) Cycling mechanism

TRIGGERING MECHANISMTRIGGERING MECHANISM

• Controlled

• Assisted

• Assist/Control

PRESSURE CYCLED PRESSURE CYCLED

• Tidal volume is affected by the flow rate, and mechanical properties of respiratory system

• Therefore, increased airway resistance or decreased compliance leads to decreased tidal volume

COMPLIANCECOMPLIANCE

• Tv/Pplateau = static effective respiratory system compliance– ~ 100 ml/cm in normals

• Tv/(Ppeak-Peep) = effective dynamic respiratory system compliance

Clinical Modes of VentilationClinical Modes of Ventilation

• 1) Controlled Ventilation– Volume or pressure controlled– A preset tidal volume or pressure and rate are

set and the patient is not allowed to take any spontaneous breaths. The original ventilators were volume control ventilators. Very uncomfortable because the patient can’t take a breath between ventilator breaths. Not used any more except in the operating room where patient is under general anesthesia.

HEMODYNAMIC EFFECTS of HEMODYNAMIC EFFECTS of Positive Pressure VentilationPositive Pressure Ventilation

• Cardiac output decreased

• Systemic blood flow decreased

• Heart rate unchanged (decreased stroke vol.)

TIDAL VOLUMESTIDAL VOLUMES

• 5-10 ml/KG

• < T ml cause hypoventilation

• If peak air way pressure exceeds 30 cm H2O, there is a decrease in tidal volume

ELEVATED PEAK PRESSUREELEVATED PEAK PRESSURE

• ? Air way resistance

• ? Reduced respiratory compliance

PLATEAU PRESSUREPLATEAU PRESSURE (occlude (occlude expiratory port at end inspiration, relaxed PT)expiratory port at end inspiration, relaxed PT)

• Represents the pressure required to hold the lungs and chest wall at the current volume (FRC + TV)

EFFECTIVE RESPIRATORY EFFECTIVE RESPIRATORY COMPLIANCECOMPLIANCE

• Tv/PL = Static effective respiratory system compliance

• 100 ml/cm in Normals

NONINVASIVE POSITIVE NONINVASIVE POSITIVE PRESSURE VENTILATIONPRESSURE VENTILATION

• BiPAP• Positive pressure ventilation delivered via

tight fitting facial mask covering• Both the nose and mouth or just the nose• Set both an inspiratory an expiratory

pressure and rate– Assists with ventilation– May allow carefully selected group of patients

to avoid intubation

NONINVASIVE POSITIVE NONINVASIVE POSITIVE PRESSURE VENTILATIONPRESSURE VENTILATION (CONTINUED)(CONTINUED)

• Problems:– Often poorly tolerated– Air leaks around mask– Skin breakdown with prolonged use– Heavy burden on nursing and respiratory staff– Need close monitoring to avoid emergency intubation– Still needs to be better studied before routine use– Has had best results in patients with chronic respiratory

failure– due to neuromuscular disease and deformities of the chest

wall