PART II

Mr. R

“His vitals are okay but he’s breathing faster than he was before.”

Mr. R

Vital Signs• Heart rate 128• Blood pressure 155/90• Respiratory rate 36• Oxygen saturation is 90% on room air

Mr. R

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Elevated pCO2 is a marker of fatigue

until proven otherwise!

Mr. R

“He’s had a few admissions for COPD

exacerbations.”

Why is he in trouble?

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Why is he in trouble?

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Why Is He in Trouble?

Increase in his Work of Breathing

Work of Breathing = Minute Ventilation

The purpose of ventilation is to eliminate CO2

Minute Ventilation (L/min) = RR x tidal volume

The brain wants a normal pH = normal pCO2 Caveat: unless it has been reset

Tidal Volume

• Tidal volume

– alveolar volume (useful) +

– dead space (useless)

Tidal Volume

• Tidal volume

– alveolar volume (useful) +

– dead space (useless)

Tidal Volume

• Tidal volume

– alveolar volume (useful) +

– dead space (useless)

Normal breathing

Normal Breathing:

At Rest:

RR of 10 breaths/minvolume of 500mL

VE = RR x VT = 10 x 500

VE of 5L/min

VE = 5 litres/min

VE = 10 litres/min

Why is exercise harder in COPD?

COPD Breathing

At Rest, ⬆WOB:VT = 500, ↑ 𝑅𝑅𝑅𝑅 = 15

VE = 7.5 L/min

250 mL

250 mL

Lung mechanics

D. E. O'Donnell, and P. Laveneziana Eur Respir Rev 2006;15:61-67

©2006 by European Respiratory Society

At Baseline:

Muscles of respiration already stretched so working from a disadvantage

During a COPD exacerbation

Increased CO2 production:⇢ COPD exacerbation⇢ Infection⇢ Anxiety

Increased dead space:⇢Increased RR in attempt to increase VE⇢Insufficient time to exhale – gas trapping

COPD and FRC

Mr. R has COPD

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Mr. RIn ER:• Gets put on FiO2 100%

by non-rebreather

What’s So Bad About That?

Adding O2 Can Only Be Better, Right?

Adding O2 increases the WOB

Beware Too Much Oxygen!Aim to correct hypoxia without reversing

hypoxic vasoconstriction

O2 saturations: 88 – 92%

Mr. R

The RT approaches you and suggests trying NIV

COPD and Respiratory FailureExpiratory flow limitation:⇢Lungs cannot empty to relaxation volume⇢Air still trapped inside the lungs = PEEPi

The best treatment would:– Offload inspiratory muscles– Allow for adequate exhalation to reduce gas

trapping and dead space ventilation

Role of Non-Invasive Ventilation

Atm P = 0

Pleural P = -5

Atm P = 0

Pleural P = -15

Trapped gas P= 10Trapped gas P = 10

Normal COPDE

⬆ WOB

PEEP = 10

Pleural P = - 5

Trapped gas P= 10

Atm P = 0

Pleural P = -15

Trapped gas P= 10Trapped gas P = 10 Trapped gas P = 10

⬇ WOB

NIV and COPD• Number needed to treat to reduce

need for intubation: 4

• Number needed to treat to reduce mortality: 10

CaveatMake sure it’s working!

Does patient look more comfortable?

Is paCO2 falling?

Is pH correcting?

Close Follow-Up

1-2 hour reassessments:– Persistent tachypnea– GCS < 11– Agitation/Fighting– pH not improving– Hypercapnea not improving

NOT WORKING

NIV and COPD

Does not apply to normocarbic

COPD!

Mr. R

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Mr. R

He was unable to tolerate NIV!

Do you have any other options?

High Flow Nasal Cannula

Who has used this before?

1. Warmed, humidified air• Comfy

2. High flow rates (up to 60 lpm) so less air entrainment

• More precise FiO2 delivery3. CO2 washout within anatomical

dead space4. High flow overcomes airway

resistance•Exact PEEP effect unclear

HFNC: Mechanisms

HFNC in Acute COPDE• NIV still considered superior

• All trials have excluded acute hypercapneicrespiratory failure

• (But we still use it here!)

Mr. R

“Wait a minute! He doesn’t have COPD!

But his last 2D echo showed an ejection

fraction of 26%!”

Mr. R has CHF

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

NIV and Congestive Heart Failure

Without PEEP

Add PEEP

1. PEEP & Venous Return

PEEP changes the natural pressure gradient in the body:

• Blood outside the thoracic cavity (positive) normally flows toward the thoracic cavity (negative)

• Now blood has to move from positive to MORE positive

2. PEEP & RV Afterload (or Pulmonary Vascular Resistance)

Hypoxic vasoconstriction

2. PEEP & RV Afterload (or Pulmonary Vascular Resistance)

Overdistendedalveoli

2. PEEP & RV Afterload (or Pulmonary Vascular Resistance)

Perfect!

2. PEEP & RV Afterload

PEEP can increase RV afterload:Alveolar overdistention and compression of vessels

PEEP can decrease RV afterloadIf there is good alveolar opening and better V/Q matching and less hypoxic vasoconstriction of alveolar vessels

TMpressure = Pressure in LV – Pressure around LV

TMpr= 100 – 20 = 80

TMpr = 100 – (-20) = 120

With PEEP

RegularBreathing

3. PEEP & LV Afterload

The positive intrathoracic pressure actually helps the LV eject by

decreasing transmural pressure (TM pressure)

PEEP decreases the pressure the LV has to work against in order to eject blood

Mr. R has CHF

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Positive Pressure and CHFNumber needed to treat to reduce endotracheal intubations: 8

Number needed to treat to reduce in-hospital mortality: 13

CPAP or NIV for CHF?Equivalent effects:

Likely the impact of PEEP rather than inspiratory muscle unloading

However:NIV better tolerated by patients

Mr. R

“Wait a minute! He doesn’t have CHF or

COPD!

But he’s febrile and bilateral infiltrates on his

CXR!”

Mr. R has Pneumonia

pH 7.25pCO2 65pO2 58HCO3 33SaO2 89

Will CPAP or NIV work here?

CPAP and NIV: The Evidence

Indication CPAP NIV Evidence LevelSevere COPD Exacerbation• pH

Hypoxemic Respiratory Failure & ARDS

Data is conflicting

• Poorer outcomes in sicker folks• Severe hypoxemia (low P/F ratio < 150)• Septic shock• Metabolic acidosis

• Level 1C evidence against using CPAP in hypoxemic respiratory failure

Hypoxemic Respiratory Failure,ARDS & NIV

• Increased work of breathing:• Increased CO2 production due to infection• Increased dead space fraction

• BUT:• Very different than COPD• This will not be a short illness

Don’t Delay a Needed Intubation!

Intubation is not a failure of therapySometimes it is the appropriate therapy

High Flow Nasal Cannula

Does it work for hypoxemia?

1. A good choice!2. Can start at FiO2 1.0 and flows

up to 60 lpm3. Watch RR, SaO2, signs of

distress, need for vasopressors

If you aren’t weaning down HFNC or your patient is getting sicker, it isn’t

working!

HFNC in Hypoxemic Respiratory Failure

1. A good choice!2. Can start at FiO2 1.0 and flows

up to 60 lpm3. Watch RR, SaO2, signs of

distress, need for vasopressors

If you aren’t weaning down HFNC or your patient is getting sicker, it isn’t

working!

HFNC in Hypoxemic Respiratory Failure

Leaving the ICU

Post-ICU: Good News!Survival from sepsis has improved!

More patients survive to hospital discharge!

Well surely there’s no downside!

What do patients look like when they leave ICU?

6 minute walk test 76% of predicted distance

Reduced physical quality of life scores

Post ICU Syndrome

Physical function

Cognitive function

Psychiatric function

Cognitive Dysfunction Post-ICU

Incidence: 25 – 78%Patients: Respiratory failure or shockAt 3 and 12 months:

40 % had deficits in keeping with Mod TBI26% had deficits in keeping with mild dementia

Cognition Dysfunction

What does this mean for my patient?

Poor memory

Poor attention and concentration

Poor executive function

Psychiatric Dysfunction

Depression

Anxiety

Post-traumatic stress disorder (ARDS in particular)

Physical disability

Critical illness myopathy

Critical illness polyneuropathy

Combined

Major Objectives: A ReviewAt the end of this session learners will be able to:Describe the key steps in

management of the septic patient Discuss management strategies for

acute respiratory failureAppreciate the burden of illness of

critically ill patients after discharge from the ICU

Thank YouNatalie WongDepartments of Medicine & Critical CareSt. Michael’s Hospitalwongn@smh.ca

Shelly DevDepartment of Critical Care MedicineSunnybrook Health Sciences Centreshelly.dev@sunnybrook.ca

mailto:wongn@smh.camailto:shelly.dev@sunnybrook.ca

PART IIMr. RMr. RMr. RSlide Number 5Mr. RWhy is he in trouble?Why is he in trouble?Why Is He in Trouble?Slide Number 10Work of Breathing = Minute VentilationTidal VolumeTidal VolumeTidal VolumeNormal breathingSlide Number 16VE = 5 litres/minSlide Number 18Why is exercise harder in COPD?Slide Number 20Slide Number 21Lung mechanicsSlide Number 23Slide Number 24During a COPD exacerbationCOPD and FRCMr. R has COPDMr. RAdding O2 Can Only Be Better, Right?Adding O2 increases the WOBBeware Too Much Oxygen!Mr. RCOPD and Respiratory FailureRole of Non-Invasive VentilationSlide Number 35Slide Number 36Slide Number 37NIV and COPDCaveatClose Follow-UpNIV and COPDMr. RMr. RHigh Flow Nasal CannulaHFNC: MechanismsHFNC in Acute COPDEMr. RMr. R has CHFNIV and Congestive Heart FailureWithout PEEPAdd PEEP1. PEEP & Venous Return2. PEEP & RV Afterload �(or Pulmonary Vascular Resistance)2. PEEP & RV Afterload �(or Pulmonary Vascular Resistance)2. PEEP & RV Afterload �(or Pulmonary Vascular Resistance)2. PEEP & RV AfterloadTMpressure = Pressure in LV – Pressure around LV3. PEEP & LV AfterloadMr. R has CHFSlide Number 60Positive Pressure and CHFCPAP or NIV for CHF?Mr. RMr. R has PneumoniaCPAP and NIV: The EvidenceHypoxemic Respiratory Failure & ARDSHypoxemic Respiratory Failure,�ARDS & NIVDon’t Delay a Needed Intubation!High Flow Nasal CannulaHFNC in Hypoxemic Respiratory FailureHFNC in Hypoxemic Respiratory FailureLeaving the ICUPost-ICU: Good News!What do patients look like when they leave ICU?Slide Number 75Slide Number 76Post ICU SyndromeSlide Number 78Cognitive Dysfunction Post-ICUCognition DysfunctionPsychiatric DysfunctionPhysical disabilitySlide Number 83Major Objectives: A ReviewThank You