RESPIRATORY FAILURE

Svetlana Plamadeala

MD, PhD, associate professor, Anesthesia and Intensive Care Department

Coordinator of training program in CUSIM

MEDPARK International Hospital, ICU and Anesthesia department

Member of examination subcommittee part I EDAIC, Republic of Moldova

sveta_plam@yahoo.com
 F RO M C L I N I C A L S E T T I N G TO C L A S S RO O M

• F, 68 yar-old
• At admition complaines:
 Chest pain
 Progressive dispnea
 Progressive weakness

• Past medical history: HT

• Past surgical history: NA
• The last 14 days patient received medications BUT without some
positive dynamic

2
 VITAL SIGNS

• A – speaking patient
• B – RR 24/min, SpO2-92 at room air, auscultative - some
crackles on the right upper part of the lung
• C – BP130/80 mmHg, HR – 87/min, Sinus rhythm
• D – aware and a bit restless
• E – nothing to remark

3
3 DAYS LATER

4
 VITAL SIGNS

• A – speaking<5 word-sentences
• B – RR 28/min, SpO2-86 at 6 L O2 through face mask,
auscultative - crackles on the area of right lung and some
in the bottom of left lung
• C – BP125/90 mmHg, HR – 112/min, Sinus rhythm
• D – aware and much more restless
• E – sweaty

5
THERE ARE SIGNS SUGGESTIVE
FOR RESPIRATORY FAILURE?

6
 1.YES

2. NO

3. MAY BE

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1.YES

8
 VITAL SIGNS

• A – speaking<5 word-sentences
• B – RR 28/min, SpO2-86 at 6 L O2 through face mask,
auscultative - crackles on the area of right lung and some
in the bottom of left lung
• C – BP125/90 mmHg, HR – 112/min, Sinus rhythm
• D – aware and much more restless
• E – sweaty

9
 HOW WE DEFINE RF?

The loss of the ability to ventilate adequately or to provide

sufficient oxygen to the blood and systemic organs. The pulmonary
system is no longer able to meet the metabolic demands of the
body with respect to oxygenation of the blood and/or
CO2 elimination.

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 CL ASSI FIC ATION R F

• Type 1 (Hypoxemic ) - PO2 < 60 mmHg on room air at

sea level

• Type 2 (Hypercapnic/ Ventilatory ) - PCO2 > 50 mmHg (if

not a chronic CO2 retainer) and a pH<7,35

• Type 3 (Peri-operative) – a subset of type 1 failure

• Type 4 (Shock) - secondary to cardiovascular instability

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 CL ASSI FIC ATION R F

• Type 1 (Hypoxemic ) - PO2 < 60 mmHg on room air at

sea level

• Type 2 (Hypercapnic/ Ventilatory ) - PCO2 > 50 mmHg (if

not a chronic CO2 retainer) and a pH<7,35

• Type 3 (Peri-operative) – a subset of type 1 failure

• Type 4 (Shock) - secondary to cardiovascular instability

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CL ASSI FIC ATION R F

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OX YG E N PAT H WAY

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OX YG E N PAT H WAY

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OX YG E N PAT H WAY

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OX YG E N PAT H WAY

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H B & OXY G EN BI NDI NG

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OXY G EN - H EMOGLOB IN DI SSOCI ATION
CURV E

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OXY G EN - H EMOGLOBIN DI SSOCI AT ION
CURV E

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 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch
• Diffusion abnormality
• Venous admixture

21
 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch
• Diffusion abnormality
• Venous admixture 22
 C AUS E S O F H YP OXE MIA

Hyper

• Low FiO2 (high altitude)

• Hypoventilation Hypo
• V/Q mismatch
• Diffusion abnormality
• Venous admixture 23
 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch (low V/Q)
• Diffusion abnormality
• Venous admixture 24
 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch
• Diffusion abnormality
• Venous admixture 25
 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch
• Diffusion abnormality
• Venous admixture
26
 C AUS E S O F H YP OXE MIA

• Low FiO2 (high altitude)

• Hypoventilation
• V/Q mismatch
• Diffusion abnormality
• Venous admixture
27
TYP E 2 ( HYP E R CAPNIC / V E N T I LATO RY )

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MAI N C AUSE S OF H Y P OV E NT I LATI ON

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30
WHICH TYPE OF RF DEVELOPED
OUR PATIENT

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 VITAL SIGNS

• A – speaking<5 word-sentences
• B – RR 28/min, SpO2-86 at 6 L O2 through face mask,
auscultative - crackles on the area of right lung and some
in the bottom of left lung
• C – BP125/90 mmHg, HR – 112/min, Sinus rhythm
• D – aware and much more restless
• E – sweaty

32
 1. HYPOXEMIC RF

2. HYPERC APNIC RF

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WHAT ELSE COULD BE HELPFUL?

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 CH E ST X - R AY

D. 1 D. 5

35
CT???

36
 ABG

• pH 7.48 Hypoxemia
• PaO2 58
• PaCO2 -26
• HCO3 – 22
• BE – 2
Hypocapnia???
• Lactate 1.2

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 L OOK S L I K E A P UL MONARY E DE MA?

Cardiogenic NON - Cardiogenic

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C AR DI OG ENIC P UL MONARY E DE MA

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NON- C AR DI OG ENIC P UL MONARY E DE MA

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 Origin
of edema

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IT IS TIME FOR TTE

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 TTE

 Hypokinezia lateral wall of LV

 Suspition on Mitral valve chordal rupture

 Severe mitral valve regurgitation

 SPAP 40 mmHg

 EF - 63%

 Bilateral pleural effusion

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 TTE

 Hypokinezia lateral wall of LV

 Suspition on Mitral valve chordal rupture

C AR
 Severe mitral D IOGENIC
valve regurgitationP UL M ONARY EDEM A

 SPAP 40 mmHg

 EF - 63%

 Bilateral pleural effusion

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 CT???

UNI L ATE RAL C ARDIOGENIC P UL M ON ARY EDEM A

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FIRST PROBLEM - HYPOXEMIA

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47
48
49
MECHANICAL VENTILATION

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51
NIV

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 CPAP
CONTINUOUS POSITIVE AIRWAY PRESSURE

53
 Dr. Sullivan essentially reversed a vacuum cleaner
motor so it would blow air into a patient's nose via
tubing. As expected, this kept the airway from
collapsing (1980). Within a few years CPAP was
commercially available in the U.S., and replaced
tracheostomy as treatment of choice for severe OSA.
Without doubt CPAP was the catalyst for widespread
development of sleep labs to diagnose OSA and for
the evolution of sleep medicine as a recognized
medical specialty.

SULLIVAN, COLIN EDWARD

Royal Prince Alfred Hospital in Sydney, Australia

Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure
applied through the nares. Lancet 1981;1:862-5

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CPAP VS SPONTANEOUS BREATHING

-5 -
-8

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 Inspiration Exhalation

+7
CPAP
+5
+3

+2
0 Spontaneous breathing
-2

CRF [0] < CRF [+5] 56

NIV IN ACUTE C ARDIOGENIC PULMONARY
EDEMA

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 IMPACT OF NIV ON RESPIRATORY
SYSTEM

• Recruits partially collapsed alveoli

• Rises FRC

• Improves oxygenation

• Decreases the work of breathing

• Improves pulmonary compliance

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IMPACT OF NIV ON RESPIRATORY SYSTEM

Reduces preload

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IMPACT OF NIV ON RESPIRATORY SYSTEM

Reduces afterload and LV work.

Decreases oxygen consumption on heart level
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IF C ARDIOGENIC ORIGIN OF PE IS
EXCLUDED…

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62
 PULMONARY CT

V>Q

V<Q
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HYPOXIC PULMONARY VASOCONSTRICTION

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WEST ZONES

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SUPINE VS PRONE

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PROTECTIVE VENTILATION

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PROTECTIVE VENTILATION

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DID YOU FORGET ABOUT OUR PATIENT?

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 CH E ST X - R AY B E FOR E SUR G E RY

D. 5 D. 7

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Ventilated NIV preoperatively
Mitral valve repair anuloplasty due to the papillary muscles rupture.
Tricuspid valve repair. By pass on LAD.

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 DYNAMIC OF PAO2/FIO2

400
350
300
250
200
150
100
50
0

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 CHEST X-RAY POP

H. 0 D. +1

D. +7

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 POSTOPERATIVELY

• Transfer from ICU on the day 4th

• Discharged from the hospital in the 8th Post-op day

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 TAKE HOME MESSAGES

• Respiratory failure – 4 types

• Hypoxemic and hypercapnic – more common

• Pulmonary edema could be cardiogenic and non-cardiogenic

• The medical approach is different for this 2 types of RF

• Timely diagnostic is lifesaving

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