Unveiling the Mysteries of Mechanical Ventilation

Nicole Kupchik MN, RN, CCNS, CCRN-K, PCCN-CMC, CSC&

Karen LaRouche’ RRT-AACS

www.nicolekupchikconsulting.com

Nicole Kupchik

MN, RN, CCNS, CCRN-K, PCCN-CMC, CSC

Nicole Kupchik has been a registered nurse specializing in Critical Care for over 25 years. She graduated nursing school in 1993 from Purdue University. In 2008 she received a Master’s Degree in Nursing specializing as a Clinical Nurse Specialist from the University of Washington Seattle.

Nicole worked as a CNS at Harborview Medical Center in Seattle, Washington and is the founder of Nicole Kupchik Consulting.

Karen LaRoche’

RRT-AACS

Karen has been a registered respiratory therapist practicing Critical Care for over 20 years. She graduated from Respiratory School in 993 and received her Adult Acute Care Specialty credential in 2013. Currently she is working as a Clinical Specialist at Harborview Medical Center Seattle, Washington.

Since 2011 Karen has been involved with both lecture and hands on mechanical ventilation education for variety of groups including respiratory therapists, critical care nurses, respiratory and nursing students, Airlift Northwest, Medic One, and countless Resident Physicians within the UW system.

Unveiling the Mysteries of Mechanical Ventilation ABG Interpretation & Capnography Nicole Kupchik

1:15:36 minutes Ventilation 101 Karen LaRoche’

1:17:06 minutes COPD Treatment Strategies Nicole Kupchik

1:05:37 minutes ARDS Management: A Case-Based Approach Karen & Nicole

58:33 minutes ARDS Management: Rescue Strategies Karen & Nicole

1:25:03 minutes

How to find us!

www.nicolekupchikconsulting.com

Facebook: Nicole Kupchik Consulting & Education Instagram: nicolekupchik YouTube: Nicole Kupchik LinkedIn: Nicole Kupchik

All rights reserved. No part of this booklet may be reproduced, stored in a retrieval system or transmitted by any other means without the written permission of

Nicole Kupchik Consulting, Inc.

THE ABCS OF ABGS…A CASE-BASED APPROACH

Nicole Kupchik MN, RN, CCNS, CCRN, PCCN-CMC

Objectives

Review normal and abnormal arterial blood gas

values

Discuss common acid/base imbalances and

treatments

Analyze case examples with treatment strategies

Discuss the integration of Capnography into care

Arterial Blood Gases

Be methodical when assessing ABGs

Look at 3 main values to interpret:

pH PaCO2 HCO3

Lungs:Fast compensation

Kidneys:Slow compensation

Compensation

Blood buffers provide immediate protection

The lungs excrete 13,000 mEq/day of volatile acid

Carbonic acid

The kidneys excrete 40 – 80 mEq/day of fixed

acid

Sulfuric & phosphoric acids

Normal Blood Gas values

Arterial Venous

pH 7.35 – 7.45 7.32 – 7.42

PaO2 80 - 100 28 - 48

PaCO2 35 - 45 38 – 52*

HCO3 22 - 26 19 - 25

Base

Excess/Deficit

- 2 to + 2

SaO2 95 – 100% 50 – 70%

Why is the venous CO2 higher than arterial?

ABG Interpretation

pH: 7.35 ----- 7.40 ----- 7.45

Acid Alkaline

PaCO2: 35 ----- 40 ----- 45

Alkaline Acid

HCO3: 22 ----- 24 ----- 26

Acid Alkaline

ABG Analysis

1. Always assess the pH first!

2. Is it normal?

3. Is there acidosis or alkalosis?

4. Which other value (PaCO2 or HCO3) is trending

with the pH?

pH: 7.28 PaCO2: 54 PaO2: 196 HCO3: 26

If PaCO2 is the cause, it’s RESPIRATORY!

If HCO3 is the cause, it’s METABOLIC

Examples:

pH 7.36 PaCO2 48 HCO3 24

Compensated Respiratory Acidosis

pH 7.26 PaCO2 35 HCO3 16

Uncompensated Metabolic Acidosis

pH 7.30 PaCO2 58 HCO3 30

Partially Compensated Respiratory Acidosis

pH 7.28 PaCO2 48 HCO3 18

Mixed Respiratory & Metabolic Acidosis

Example:

pH 7.52 PaCO2 26 HCO3 22

Uncomp. Respiratory Alkalosis

_______ _______ _______

Respiratory Alkalosis Causes

Early respiratory failure

Anxiety or severe pain

Excessive tidal volume or rate on ventilator

ARDs

Heart failure

Neurologic disorders/CVA

Acute onset can cause cerebral vasoconstriction

Pulmonary embolus

Salicylate overdose (adults)

Decreased Cardiac Output/Shock (↑ RR)

PaO2 < 60 (Cause & effect)

Fever

Panic disorders

Pneumo/Hemothorax

Aspiration

Asthma/emphysema

Sepsis

Hepatic failure

Think hyperventilation! (blowing off CO2)

Example:

pH 7.22 PaCO2 65 HCO3 24

Uncomp. Respiratory Acidosis

_______ _______ _______

Respiratory Acidosis Causes

Late respiratory failure

Over-sedation

Drug overdoses that cause respiratory depression

Acute pulmonary edema

Lung diseases

Asthma, COPD/emphysema

Brain stem dysfunction

Extreme V/Q mismatch

Pulmonary embolus, PNA

Guillain Barre’

Excessive CO2 production (Sepsis, TPN, Burns)

Severe obesity

Muscle weakness

Cardiac arrest

Think hypoventilation! (retaining CO2)

Acute Respiratory acidosis – Medical emergency

Chronic – Body adapts, kidneys produce HCO3 to compensate

Example:

pH 7.16 PaCO2 35 HCO3 14

Uncomp. Metabolic Acidosis

_______ _______ _______

Metabolic Acidosis Causes

Acute kidney injury

Drug & alcohol overdoses

Diabetic Ketoacidosis

Sepsis

Lactic Acidosis

Toxins

Aspirin overdose

Liver failure

Hyperkalemia

Hyperchloremia

Calculate an anion gap!!!

Either body produces too much acid, OR

Kidneys aren’t getting rid of it

Suppresses myocardial contractility

(↓ CO, ↓ BP)

Anion gap: Normal < 11 - 12

Na++ Cl-

K+ (don’t count) HCO3-

> 12 associated with metabolic acidosis

M: Methanol P: Propylene glycol

U: Uremia I: Isoniazid

D: DKA L: Lactic acidosis

E: Ethylene glycol

S: Salicylates

Example:

pH 7.49 PaCO2 36 HCO3 29

Uncomp. Metabolic Alkalosis

_______ _______ _______

Metabolic Alkalosis Causes

NG tube to suction

Vomiting/emesis

Hypokalemia

Hypochloremia

Antacid abuse

Excessive sodium bicarb infusion

Inadequate renal perfusion

Thiazide & loop diuretics

Excessive albuterol use

Hyperaldosteronism (d/t RAAS activation)

Too much bicarb in the blood OR,

Loss of chloride

Vomiting – loss of stomach acid

Practice:

pH 7.50 PaCO2 28 HCO3 24

Uncomp. Respiratory Alkalosis

_______ _______ _______

Causes: Hyperventilation, early respiratory failure,

Anxiety, excessive tidal volume on vent

Practice:

pH 7.51 PaCO2 35 HCO3 32

Uncomp. Metabolic Alkalosis

_______ _______ _______

K+ 2.1 – 27 y.o., recovering sepsis, 30+ pounds fluid

overload, diuresing 200 – 400 ml/hr

Practice:

pH 7.24 PaCO2 87 HCO3 26

Uncomp. Respiratory Acidosis

_______ _______ _______

Causes: Hypoventilation, Late respiratory failure,

over-sedation, brain stem dysfunction

Practice: Patient with bacterial infection

pH 7.49 PaCO2 28 HCO3 24

Uncomp. Respiratory Alkalosis

_______ _______ _______

Causes: Sepsis – Pneumonia with RR 30s

Practice: Aspirin overdose

pH 7.31 PaCO2 22 HCO3 18

Partially Comp. Metabolic Acidosis

_______ _______ _______

Cause: Salicylate level = 889 mg/LModerate toxicity occurs at doses up to 300 mg/kg, severe toxicity occurs between

300 to 500 mg/kg, and a potentially lethal dose is greater than 500 mg/kg

Practice: Post operative patient just

admitted from the PACU

pH 7.28 PaCO2 52 HCO3 26

Uncomp. Respiratory Acidosis

_______ _______ _______

Causes: Hypoventilation, over-sedated

Practice: Septic patient with lactate 4.8

pH 7.32 PaCO2 28 HCO3 17

Part. Comp Metabolic Acidosis

_______ _______ _______

Causes: Hypo-perfused in the state of sepsis

Practice: Type 1 Diabetic presenting with sepsis

pH 7.26 PaCO2 28 HCO3 14

Part comp. Metabolic Acidosis

_______ _______ _______

Causes: Ketoacidosis, check the potassium

Case study

You admit a 49 year old Type 1 Diabetic who is

admitted with LOC changes.

Labs:

Na 132, K+ 6.5, PO4 1.3, glucose 483, + large

amount ketones blood & urine, anion gap = 22

ABG: pH 7.12/ PaCO2 24/ PaO2 85/ HCO3 14

Your interpretation?

Partially Compensated Metabolic Acidosis

Acidosis in Hyperglycemia

For every 0.1 ↓ in pH

pH 7.3

pH 7.2

pH 7.1

pH 7.0

pH 6.9

0.6 ↑ in serum K+

K+ 4.6

K+ 5.2

K+ 5.8

K+ 6.4

K+ 7.0

K+ & pH have an inverse relationship

62 year old has the following ABG:

pH: 7.36 PaCO2 58, PaO2 62, HCO3 28

The patient likely has:

A. Uncompensated respiratory acidosis

B. Compensated respiratory alkalosis

C. Acute kidney injury

D. COPD

E. Acute myocardial infarction

A patient with ESKD presents with mental status changes after he skipped

dialysis for 3 days. His ABG reveals the following: pH 7.12/ PaCO2 32/

PaO2 180/ HCO3 18. After analyzing the results, you know the patient has:

A. Uncompensated respiratory alkalosis

B. Partially compensated respiratory acidosis

C. Uncompensated metabolic alkalosis

D. Partially compensated metabolic acidosis

A patient with the following ABG needs additional

diuresis. Has been receiving 120 mg furosemide daily x

5 days.

A. Uncompensated respiratory alkalosis

B. Partially compensated respiratory

acidosis

C. Uncompensated metabolic alkalosis

D. Partially compensated metabolic

acidosis

ABG results:

pH 7.51 / PaCO2 42 / PaO2 108 / HCO3 36

Which of the following would be the diuretic of

choice in a persistent metabolic alkalosis?

A. Diuril (thiazide)

B. Additional furosemide (Loop)

C. Torsemide (Loop)

D. Acetazolamide / Diamox

E. Edecrin (Loop)

Capnography

Carbon dioxide

What you exhale

Normal: 35 – 45 mmHg

(V = ventilation)

What you measure in the arterial

blood

Normal: 35 – 45 mmHg

(Q = Perfusion)

The relationship between them is V/Q

This Photo by Unknown Author

is licensed under CC BY-SA

Continuous Waveform Capnography

Waveform Capnography

Endotracheal tube verification

Level 1A recommendation from AHA/ILCOR

Normal PEtCO2 = 35 – 45 mmHg

Correlates with PaCO2 in normal V/Q relationships

< 5 mmHg difference

When to use Waveform Capnography?

When an endotracheal tube is placed

Procedural, moderate to deep sedation

High risk patient on PCA

Gold standard for endotracheal tube placement

Cardiac arrest

Quality indicator of compressions

Information helpful to determine cessation of

resuscitation efforts

Post arrest

PCA pumps now have Capnography!

This Photo by Unknown Author is licensed under CC BY-SA

Case #1

You are asked to administer procedural sedation to

a patient who is experiencing a GI Bleed for an

endoscopy procedure

The patient is not intubated, but has been

experiencing hypotension

Current VS: HR 128 bpm, BP 92/48, RR 26, O2 sat

92% on 40% venti mask

Case #1 continued

The patient is noted to have a large neck with

questionable OSA history (doesn’t use CPAP at home)

You are asked to administer 2 mg IV midazolam & 100

mcg Fentanyl to start

What type(s) of monitoring would you like for the

endoscopy?

Continuous Waveform Capnography!!!

Case #1 Continued

Baseline EtCO2 is 38 mmHg

Midazolam & Fentanyl are administered

The patient is placed on his side, getting sleepy, but

is still easily arousable

EtCO2 is 40 mmHg

What would you like to do?

Case #1 Continued

Midazolam 2 mg administered with another 100 mcg of Fentanyl IV

EtCO2 is now 49 mmHg

What would you like to do?

Stay the course – An increase in PEtCO2 of 20 –25% is reasonable!

American Society of Anesthesiologists

National standard mandate

Ventilation should be monitored via etCO2 for all

patients receiving moderate to deep sedation who

are not intubated.

Since 2010!

Case #2

65 year old patient with sepsis

Intubated & now hypotensive:

HR 102, BP 84/42, Vented rate 16, breathing 22, O2 sat 94%

Has a central line in place

CVP 12 mmHg

Treatment: Fluids, pressors or inotrope?

ETCO2 predicts fluid responsiveness

in passive leg raising

65 ventilated patients needing volume expansion

Compared changes in EtCO2 with arterial pressure to reflect

changes in CO

EtCO2 increase ≥ 5% predicted fluid responsiveness (p=0.0001)

Increase in the CI ≥ 15%

Sensitivity 71% (95% CI 48 – 89%) and specificity of 100%

(CI 82 – 100%)

The changes in EtCO2 induced by a PLR test predicted fluid

responsiveness with reliability, while the changes in arterial pulse

pressure did not.

This Photo by Unknown Author is licensed under CC BY-NC-ND

Passive leg raising

Legs elevated for 1 to 2 minutes

Re-evaluate – ideally stroke volume measure

Transfer of blood from legs

and abdominal compartment

This Photo by Unknown Author is licensed under CC BY-NC-ND

Passive Leg Raising

Patient – HOB 45 degrees

Obtain Capnography reading

Capno: 32 mmHg

Lift legs for 1 – 2 minutes

Capno reads 38 mmHg after 90 sec

What does the patient need?

Fluids!!!!!

This Photo by Unknown Author is licensed under CC BY-NC-ND

Case

49 year old female s/p bowel resection surgery a week ago

Transferred to acute care and developed a LLE DVT

Has been on a Heparin infusion for 8 hours

PTT 52 seconds

C/O shortness of breath with increasing O2 needs and “feel

like I’m going to die”

Rapid response activated

HR 122, BP 92/46, RR 42

O2 sats quickly dropping, in the 80s

On 100% NRB mask

Gets tachycardic, 12 Lead ECG

Getting confused, struggling to breath

Goes into PEA Arrest

Chest compressions started

Your differential?

Your differential?

A. Acute Inferior Wall MI

B. Pulmonary Edema

C. Pulmonary Embolism

D. Pneumonia

Pulmonary embolism

rtPA 100 mg ordered & given

Intubated without interrupting chest compressions

EtCO2 reads 8 mmHg

CPR quality is incredible!!!

Why is it only reading 8 mmHg?

This Photo by Unknown Author is licensed under CC BY-NC-ND

Damage

V/Q relationship

She has a V/Q mismatch

What will happen to serum

arterial levels of CO2?

V/Q Mismatch

Pulmonary embolism = lots of dead space

Dead space = volume of air inhaled that does not take part in gas exchange

V = air reaches alveoli, Q = blood reaches alveoli

If the dead space is < 30%, it is considered normal

< 30%, not a PE, 100% negative predictive value

Calculation:

(PaCO2 – EtCO2) ÷ PaCO2

Calculation:

(PaCO2 – PetCO2) ÷ PaCO2

Example #1:

ABG: pH 7.32, PaCO2 49, PaO2 145, HCO3 22

EtCO2 = 44 mmHg

(49 – 44) = 5 ÷ 49 = 0.10 or 10%

Example #2:

ABG: pH 7.24, PaCO2 64, PaO2 65, HCO3 19

EtCO2 = 24 mmHg

(64 – 24) = 40 ÷ 64 = 0.625 or 62.5%

rtPA infusing, pulse returned!

Resuscitated, currently on 100% FiO2

pH 7.20, PaCO2 86, PaO2 65, HCO3 20

EtCO2 11 mmHg

What ventilator settings do you want to place the patient on?

Female, height 5’6”

Vt – 8 cc/kg (474 cc)

Rate – 18

FiO2 – 100%

PEEP – 5

Minute ventilation – 8.5 L/min (normal 6 L/min)

Case continued (PaCO2 – PetCO2) ÷ PaCO2

EtCO2 up to 11 mmHg after we achieved ROSC

rtPA infusing

Calculate deadspace:

pH 7.20, PaCO2 86, PaO2 65, HCO3 20

EtCO2 11 mmHg

What is the deadspace?

What is her deadspace?

A. 6%

B. 50%

C. 77%

D. 87%

PaCO2 = 86 mm Hg

EtCO2 = 11 mm Hg

Case continued (PaCO2 – PetCO2) ÷ PaCO2

EtCO2 up to 11 mmHg after we achieved ROSC

rtPA infusing

Calculate deadspace:

pH 7.20, PaCO2 86, PaO2 65, HCO3 20

EtCO2 11 mmHg

What is the deadspace?

87%

What would you like to do?

Is EtCO2 useless in this case?

2 hours later

pH 7.28, PaCO2 68, PaO2 85, HCO3 22

Vt – 8 cc/kg (474 cc)

Rate – 18

FiO2 – 100%

PEEP – 5

Minute ventilation – 8.5 L/min

EtCO2 is now 15 mmHg, PaCO2 68, on FiO2 100%

What is her deadspace?

A. 6%

B. 50%

C. 77%

D. 87%

PaCO2 = 68 mm Hg

EtCO2 = 15 mm Hg

2 hours later

pH 7.28, PaCO2 68, PaO2 85, HCO3 22

Vt – 8 cc/kg (474 cc)

Rate – 18

FiO2 – 100%

PEEP – 5

Minute ventilation – 8.5 L/min

EtCO2 is now 15 mmHg, PaCO2 68, on FiO2 100%

Dead space = 77%

Any changes to ventilator settings?

6 hours later…

pH 7.32, PaCO2 48, PaO2 142, HCO3 26

Vt – 8 cc/kg

Rate – 18

FiO2 – 100%

PEEP – 5

Minute ventilation – 8.5 L/min

6 hours later EtCO2 was 24 mmHg, PaCO2 48, on FiO2 100%

What is her deadspace?

A. 6%

B. 50%

C. 77%

D. 87%

PaCO2 = 48 mm Hg

EtCO2 = 24 mm Hg

6 hours later…

pH 7.32, PaCO2 48, PaO2 142, HCO3 26

Vt – 8 cc/kg

Rate – 18

FiO2 – 100%

PEEP – 5

Minute ventilation – 8.5 L/min

6 hours later EtCO2 was 24 mmHg, PaCO2 48, on FiO2 100%

Dead space = 50%

Any changes to ventilator settings?

12 hours post arrest…

pH 7.48, PaCO2 32, PaO2 248, HCO3 32

Vt – 8 cc/kg

Rate – 18

FiO2 – 80%

PEEP – 5

Minute ventilation – 8.5 L/min

12 hours later EtCO2 30 mmHg, PaCO2 32, on FiO2 80%

What is her deadspace?

A. 6%

B. 50%

C. 77%

D. 87%

PaCO2 = 32 mm Hg

EtCO2 = 30 mm Hg

12 hours post arrest…

pH 7.48, PaCO2 32, PaO2 248, HCO3 32

Vt – 8 cc/kg

Rate – 18

FiO2 – 80%

PEEP – 5

Minute ventilation – 8.5 L/min

12 hours later EtCO2 30 mmHg, PaCO2 32, on FiO2 80%

Dead space = 6.25%

Any changes to ventilator settings?

EKOS Catheter – FDA approved May 2014

This Photo by Unknown Author is licensed under CC BY-SA

EKOS Catheter

EkoSonic® catheter

Controlled infusion of thrombolytics

≥ 50% clot burden in one or both main pulmonary

arteries or lobar pulmonary arteries

Evidence of right heart dysfunction based on right

heart pressures (mean PAP ≥ 25mmHg) or

echocardiographic evaluation

Prognosis?

Good! The rtPA lysed the blood clot

This is evidenced by the improvement in the

V/Q mismatch!

In conclusion…

ABGs are NOT difficult to interpret

It takes some practice & some memorization

I hope this increased your confidence for the next time you have to interpret an ABG!!!

Consider using Capnography!

Thanks!!!

Case

58 year old admitted with pneumonia

HR 126, BP 84/52, RR 32, SaO2 85% on 4 L NC

Initial lactate 2.8

Given fluids, antibiotics

ABG: pH 7.48/ PaCO2 30/ PaO2 62/ HCO3 24

Your interpretation?

Uncompensated Respiratory Alkalosis

3 hours later…

The patient is tiring and getting more lethargic & sleepy

Repeat lactate 5.2 after a total of 5 L of fluid

ABG: pH 7.26/ PaCO2 58/ PaO2 52/ HCO3 20

Your interpretation?

Uncompensated Mixed Respiratory/Metabolic Acidosis

Moderate hypoxemia

What does the patient need at this point?

What should we do now?

Intubate/mechanically ventilate

This patient is high risk for:

ARDS!!!

Vent settings:

AMV rate 14, ~8 cc/kg TV, +5 PEEP, 60% FiO2

Post intubation:

ABG: pH 7.30/ PaCO2 52/ PaO2 68/ HCO3 24

Your interpretation?

Uncompensated respiratory acidosis

Next steps?

Vent settings:

AMV rate 14, ~8 cc/kg TV, +5 PEEP, 60% FiO2

Post intubation:

ABG: pH 7.30/ PaCO2 52/ PaO2 68/ HCO3 24

2 issues: Hypoxemic & retaining CO2 (hypo-ventilating)

Increase the set vent rate, assess the tidal volume

Increase the PEEP

Calculate the P/F Ratio

PaO2 68/FiO2 .60 = 113

Next steps?

ABG: pH 7.30/ PaCO2 52/ PaO2 68/ HCO3 24

Vent settings:

AMV rate 14, ~8 cc/kg TV, +5 PEEP, 60% FiO2

Changes:

AMV rate 18, ~6 cc/kg TV, +10 PEEP, 70% FiO2

ABG after changes:

ABG: pH 7.34/ PaCO2 48/ PaO2 72/ HCO3 26

Uncompensated Respiratory Acidosis

Increase the vent rate or possibly hold

Increase PEEP/Consider proning

P/F Ratio: 72 / .70 = 102

Karen LaRoche’, RRT-ACCS

VENTILATION 101

Objectives

Review some basic pulmonary mechanics

Compare pressure vs volume ventilation and what

classic modes are in each category

Discuss ventilator measurements and how to apply

them to patient care

Recognize the relationship of ventilation and

perfusion

Identify what role PEEP plays in mechanical

ventilation

Are you a positive pressure ventilator or a

negative pressure ventilator by design?

A. Positive

B. Negative

C. Depends on what your altitude is

Answer:

We are negative pressure ventilators by design.

This Photo by Unknown Author is licensed under CC BY-SA

Positive Pressure Ventilation

Anytime you add pressure to a patient’s lungs it’s

considered positive pressure ventilation.

CPAP (Continuous Positive Airway Pressure)

BiPAP (Bi-phasic Positive Airway Pressure)

Pressure Support

Volume control

Pressure control

ALL modes of ventilation, spontaneous or otherwise

The Big Picture

The vent "treats" nothing

Supportive in nature

Should be used as little as necessary

Mode of ventilation not as important as you would

think

277 technically different modes of ventilation

Ventilation "plan" more important

Understanding how to move through that plan most

important

Where to start?

Is there a set respiratory rate or is my patient breathing spontaneously?

Spontaneous modes

◼ Pressure Support

◼ CPAP

◼ Volume Support

If there is a set respiratory rate:

Are we setting volumes for each breath?

Are we setting pressures for each breath?

Good News!

Only 2 basics ways to target ventilation!

Set Vt

Fixed flow

Vent will do whatever it takes to deliver that volume regardless of compliance or resistance

PIP will vary

Set a PIP

Variable flow

Vent will maintain that pressure and volume will vary according to compliance and resistance

Volume Pressure

Volume Control

Pressure Control

Pressure Support

APRV

Pressure

Regulated

Volume Control

SIMV

Pressure vs. Volume?

• Systematic review and meta-analysis of 34 independent studies

• Compared all forms of Pressure ventilation including APRV & IRV

• Included ARF and ARDS patients

(2015)

Results

No significant difference in…

Pulmonary compliance

P/F ratio

PaCO2

Hemodynamics, MAP and Cardiac Index

Patient Work of breathing

◼ Noted a difference if inspiratory flow was inadequate for

patient needs on volume control

◼ When appropriately matched to patient need and similar to

flows achieved in PC, there was no difference

Volume Control: aka AMV,AC,(s)CMV

Set tidal volume

Set respiratory rate

Fixed flow ( flow rate)

Patient can assist but vent will always deliver set tidal

volume

Both PIP and Plateau pressures will change with

changes in lung compliance and chest wall compliance

Inspiratory time is fixed according to flow rate

Higher the flow rate the faster the inspiration

Pressure Control: PC

Set a preset pressure

Set a RR

Flow will be variable from breath to breath

Patient can assist but each breath will be at the set

pressure

Tidal volumes will change with changes in lung and

chest wall compliance

Pressure Regulated Volume Control: aka PCVG, Volume Guarantee, PRVC

• Marriage between PC

and Volume Control

• Tidal volume determined

by preset pressure

however pressure levels

titrated to achieve a

“goal” volume

• “RT in a box”

Modes: SIMV (synchronized

intermittent mechanical ventilation)

Set RR

Set either tidal volume

or pressure target

Patient can breathe

spontaneously

between each set vent

breathe

Are you using APRV or Bi-Level at

your institution??

A. Yes

B. No

C. I’m not sure

APRV

(Airway Pressure Release Ventilation)

“Bi-phasic CPAP” two levels of CPAP

Vent cycles between two levels at a preset rate

Vent operates independently of patient efforts

Patient MUST be spontaneously breathing.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732103/figure/F0001/

Which mode is best????

Whatever mode is most well known by bedside

practitioners at your institution

Ventilation strategies according to disease a better

way to focus care, pick a mode that best does that

particular strategy… may be all of them will work.

Match physiology with how the mode works

22 year old male admitted to ED after overdose of

OxyContin. No previous medical history known.

Patient is 5’10” (70 kg PBW), vital signs all within

normal limits

Not intubated, unarousable with RR 6

On 6 L NC with SpO2 96%

EtCO2 54

What should we do next?

A. Non-invasive ventilation

B. Intubate and mechanically

ventilate

C. Nothing, he's totally fine

Which mode of ventilation do you

think would be most appropriate?

A. Volume Mode such

as Assist Control

B. Pressure Control

mode

C. Pressure Support

Vent Settings

Things we set…

Tidal Volume or

Pressure control

level

RR

PEEP

FiO2

Other parameters

to consider…

Inspiratory flow

rate

Inspiratory time

I:E ratio

Parameters we monitor

Peak inspiratory pressure

Plateau or static pressure

Mean airway pressure

Total RR

I:E ratio

Auto-PEEP

All of these are very dynamic and change as your patient changes.

Will our 22 year old, 5'10", 180 lb overdose have the

same lung capacity and require the same tidal volume as

another 5'10”, 250 lb male?

A. Yes

B. No

Answer

Yes. Our lung capacity is based on our height and gender, not our weight.

◼Predicted Body Weight (PBW) formula:

◼Females: 45.5 + (Height in inches – 60 x 2.3)

◼Males: 50 + (Height in inches – 60 X 2.3)

A good starting point for Tidal Volume is 8-10cc/kg PBW

Predicted Body Weight Charts

Our patient is now on a Volume control mode,

what other settings would you like?

A. Vt 560, RR 12, +5 PEEP

B. Vt 900, RR 15 +5 PEEP

C. Vt 560, RR 20, +5 PEEP

Answer

A. Volume Control mode , Vt 560, RR 12, +5 PEEP

560= 8cc/kg PBW, RR 12 x 560 = VE 6.7 lpm

B. Volume Control Mode, Vt 900, RR 15 +5 PEEP

900= 13cc/kg PBW, RR 15 x 900 = 13.5 lpm

C. Volume Control Mode, Vt 560, RR 20, +5 PEEP

560= 8cc/kg PBW, RR20 x 560= 11. 2 lpm

Inspiratory and Expiratory Time

Inspiratory time: time for inspiration Usually fixed by either a set flow rate or a specific inspiratory time on

vent

Good point to start is .8seconds or around 60 LPM flow, adjust for patient comfort

Expiratory time: time for exhalation Is dynamic and effected by

◼ Changes in I-time

◼ Changes in RR

I:E Ratio Ratio of time spent on inspiration: time spent on exhalation

◼ I:E ratios of 1:2 or greater are desired

General guidelines to consider

If you want to affect the PaCO2 change your RR or

tidal volume

Increase RR or volume to blow off more PaCO2

Decrease RR or volume to raise PaCO2

If you want to affect your PaO2 change your PEEP or

FiO2

If you want to change your I:E ratio change your flow

or I-time

Minute Ventilation

Minute ventilation (VE)

RR x tidal volume (VT)

Expressed in l/min

◼ RR 12 x 500ml = 6000 ml= 6.0 L/min

Manipulation of your VE will affect your PaCO2 and

subsequently your pH

Important to keep in mind

◼ Is it high or low?

◼ How much work is it taking to maintain?

◼ Is it disproportionate for the ABG???

24 year old female post op appendectomy. Remains intubated and

on a ventilator with a total RR of 26 and a Vt 500, for a total Ve of

13.0 LPM. ABG results of 7.39, PaCO2 42, PaO2 89, HCO3 24.

A. Yes

B. No

Is this a disproportionate amount of minute

ventilation(VE) for this ABG?

Answer

YES.

Minute Ventilation “norms”

At rest, normal, not intubated = 4 - 6 LPM

Intubated and mechanically ventilated = < 10 LPM

Our patient has a high VE with a normal PaCO2

Case Study

24 year old female post fixation of a femur fracture. Remains

intubated and on a ventilator with a total RR of 26 and a tidal

volume of 500 for a total VE of 13.0 LPM, FiO2 .80 and PEEP

+5.

ABG results: 7.39 PaCO2 42 PaO2 89 HCO3 24.

Questions to ask…

• Is this minute ventilation normal?

• Is this blood gas “normal”

• Is this a relatively high minute ventilation for

this blood gas?

• Is this a relatively low PaO2 for this FiO2?

Given the patient’s history of a long bone fracture, increased

minute ventilation requirement with a “normal” PaCO2, and

relatively low PaO2 for FiO2 delivered, she is showing signs of:

A. Increased dead space and should have PE as

a high differential

B. Increased shunt and is likely to have a new

pneumonia

C. Developing ARDS

Ventilation & Perfusion

Disruption of either side can affect the transfer of CO2

into the lungs and the delivery of oxygen to the tissues.

Ventilation Defects (Shunt)

SHUNT

Ventilation is interrupted or not

efficient but perfusion is OK

V-/Q+.

Unoxygenated blood goes back

to periphery

• Major atelectasis

• ARDS

• Pneumonia

• Lobar collapse

What that looks like

Clinical picture

Tachypnea

Hypoxia that improves with increased oxygen

ABG shows high PaCO2 and low PaO2

PEEP may help

Clinical example collapsed lobe

Inhaled pulmonary vasodilators may also help if refractory to oxygen and PEEP.

◼Vasodilate the capillary membranes that surround the alveoli that ARE functioning, optimizing what is working

Perfusion Defects: Dead space

Ventilation continues but perfusion is

limited.

+V/-Q

• Classic dead space is a

Pulmonary embolism (PE)

• Over distended alveoli with too

much PEEP, squishes capillaries

• Low perfusion to pulmonary

arteriesDead space

What that looks like

Clinical picture

Tachypnea (increased VE)

If hypoxic, slow to respond with increased FiO2

if much improvement at all

ABG will show a “normal” or high PaCO2 with a

disproportionate amount of VE

24 year old Asthmatic gets intubated due to status Asthmaticus. Her

peak inspiratory pressure (PIP) on the vent are 35 but her plateau

pressure has remained the same at 20. This is a sign of …

A. Increased airway resistance

B. Increased pulmonary compliance

C. A need for ECMO

What do these numbers tell us?

Total system pressure

◼ Can be affected by …

◼ ETT size

◼ Vent flow rate

◼ Constricted airways

◼ Secretions

◼ Water in tubing

◼ Bronchospasm

Reflects both resistance in

airways and compliance of chest

◼ “normal” number generally

< 30 cm H20

Measured with “no flow” and a

fully inflated lung

Reflects only the compliance of

the chest

◼ Chest wall

◼ Lungs

◼ “normal” number in high teens

◼ Number is used to calculate

lung compliance

◼ Vt(ml)/plateau-PEEP(cm H20)

Peak inspiratory pressure

(PIP)

Plateau pressure

(Static pressure)

Dynamic Ventilator Measurements

Resistance

The resistance to airflow during inspiration

Affected by

◼ Airway size

◼ Ventilator flow rate

◼ Mechanical obstructions

◼ Secretions

◼ Inflammation in airways

Dynamic Ventilator Measurements

Compliance

Defined as a measure of the ease of expansion of the

lungs and thorax

Tidal volume(ml)/plateau pressure –PEEP (cm H20)

“normal” value on ventilator is around 50

Lower the value the stiffer the lungs

Effected by

◼ Changes in lung tissues

◼ Changes in chest wall

24 year old asthmatic intubated for 24 hours has

received aggressive bronchodilators and steroids.

A. Resistance

B. Compliance

C. Both

Her PIP are now down to 22 from 35, and plateau (static)

pressures 17 from 20.

These numbers represent an improvement in her…

PEEP

• Increases Alveolar surface area for gas exchange

to occur

• Can Decrease physiologic dead space

• May decrease WOB

• May increase lung compliance

• May effect V/Q matching

• Can allow you to deliver less FiO2

How much PEEP???

“physiologic” PEEP

Typically the 5 cm H2O everyone seems to get

PEEP to improve oxygenation

Enough to give you your desired PaO2 targets

PEEP to improve physiology

Stent open collapsible airways as used in COPD

◼ Typically 5 - 10 cm H2O

Decrease cardiac pre-load as used in CHF

◼ Typically 5 -10 cm H2O

PEEP for Protection???

Biotrauma: innate immune response to a

biological insult

Cyclical opening and closing of lung tissue

from collapsed state to over stretched states

increase biotrauma

Atelectrauma: the cyclical opening and

closing of collapsed alveoli

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1175867/pdf/cc3022.pdf

How Much PEEP???

PEEP for protection???

Stiff chest wall conditions

◼ Morbid obesity

◼ “average” is 10 cm H2O

◼ Circumferential injuries

◼ As seen in burns, patients with tight chest bracing, etc.

◼ Chest wall deformities Recruit lung, increase compliance,

improves V/Q matching

ARDS

◼ Protects from “atelectrauma”

Morbid Obesity and Lung Function

Reduced total lung capacity

Reduced Vital Capacity

Low FRC increases risk for expiratory

airflow obstruction

PEEP chosen by providers was on average 9.1 cm

H2O lower than PEEP levels required

Recruitment maneuvers were effective in this patient

population

Higher PEEP levels in this population improve

oxygenation with little impact on Hemodynamics

Critical Care Medicine: February 2016 - Volume 44 - Issue 2 - p 300–307

PEEP…the dark side…

Too much PEEP can…

Over distend alveoli

Decrease capillary blood flow and worsen V/Q

matching

Increase chance of volutrauma

Decrease venous return to right side of heart

◼decrease pre-load when pre-load reduction is not wanted

Case Study

56 year old male admitted for respiratory failure secondary to a

necrotizing pneumonia in RLL. He is 65 kg PBW. Pt is intubated

on following settings:

Volume Control , set Vt 520 ml, RR 22, PEEP +8 cm H20, 80%

FiO2

ABG 7.32 / PaCO2 62 / PaO2 60 / HCO3 29

VS: HR 115, BP 115/65, Temp 38˚C

BS coarse rhonchi throughout with bronchial sounds over RM and

RLL

What vent changes do you want to

make?

A. Increase FiO2 to 100% because his PaO2 is

low

B. Increase PEEP because his PaO2 is low and

his FiO2 is high

C. No changes, this looks good

Case Study

PEEP is increased to 15 cm H2O and FiO2 remains at 80%

Within 5 minutes of the change the patients HR increased to 140

and he becomes hypotensive with BP 75/50.

Over the next few minutes the patient begins to desaturate to

75%.

BS are equal and bilateral and ventilator pressures (PIP and

Plateau) are unchanged.

A CXR is obtained

The clinical changes in the patient are

most likely secondary to:

A. Pneumothorax

B. Sudden ARDS

C. Decreased preload due to increased PEEP

D. Rebound effect due to oxygen toxicity

When PEEP Is Bad…

Unilateral lung disease

PEEP goes to more compliant regions, over distends

them squishing capillary beds which decreases venous

return ( pre-load)

Patient becomes tachycardic, hypotensive, and may

desaturate further

BAAAAD COPD

Over distends already hyper-inflated lungs

Decreases capillary blood flow and changes v/q

matching

How much PEEP is enough PEEP?

Consider the origination of pulmonary disease

Body habitus

Underlying disease

Enough PEEP to Improve oxygenation

Improve compliance

Stent open collapsible airways

Not so much to

Decrease venous return

Over distend good alveoli

Worsen marginal pulmonary compliance

What to do if you have too much???

Dial it down…

Maximize pre-load

Does the patient need more fluid?

Does the patient need a positive

inotrope (ie. Dobutamine)

HOW MANY CHEST TUBES DO YOU SEE???

6

This Photo by Unknown Author is licensed

under CC BY-SA

Auto-PEEP

Anything that decreases

expiratory airflow can cause

auto-PEEP:

• Bronchospasm

• Inflammation in airways

• Tumor

• Too much VE

• do not allow enough time

to exhale

Incomplete exhalation resulting in trapped air at end of exhalation

How To Find Auto-PEEP On The Vent

Identifying Auto-PEEP using Pressure

waveform

Identifying Auto-PEEP using flow

waveform

This Photo by Unknown Author is licensed under CC BY-NC-SAThis Photo by Unknown Author is licensed under CC BY-NC-SA

Remember: A Delicate Balance of

Ventilation to Perfusion (V/Q)

Adequate gas exchange in the alveoli is dependent upon the appropriate matching of the amount of ventilation in the alveoli…

…and the amount of blood

flow surrounding the alveoli.

Auto-PEEP can disrupt this

delicate balance

Our next session

What’s the evidence in ARDS

management?

Non-Invasive Ventilation

COPD TREATMENT STRATEGIES

Objectives

Discuss current treatment strategies for COPD

Discuss rescue strategies for the decompensating

COPD patient

Guidelines – GOLD Initiative

Global Initiative for Chronic Obstructive Lung

Disease

Collaborative of the NIH & WHO

goldcopd.org

Chronic Obstructive Pulmonary Disease (COPD)

Umbrella term for emphysema & chronic bronchitis

Over 24 million Americans with COPD

Constant airflow obstruction

Worsens over time

Shortness of breath

Cough, +/- Sputum

Source: Global Initiative for Chronic Obstructive Lung Disease

COPD vs. Asthma

• Onset in mid-life

• Symptoms slowly

progressive

• Long smoking history

• Onset early in life (often childhood)

• Symptoms vary from day to day

• Symptoms worse at night/early morning

• Allergy, rhinitis, and/or eczema also present

• Family history of asthma

COPD Asthma

COPD - Emphysema

Air-trapping with chronic hyperinflation of lungs

Prolonged exhalation

Barrel chest

Enlarged right heart

Elevated right sided venous pressures (CVP)

Diagnostics

Pulmonary Function Test

History of smoking (85% of patients)

FEV1/FVC < 70% in COPD

FEV1: Forced expiratory volume over first 1 second

FVC (Forced vital capacity): Total volume exhaled

*Must give bronchodilator first!

Results vary by age, gender & height

Normal FEV1 is at least 70% of FVC

◼ Expressed as % predicted

◼ COPD patients take longer to exhale – airflow limitation/obstruction

Stages of COPD

goldcopd.org

COPD Stages I: Mild COPD

Stage 1

80% Normal Lung Function

COPD Stages II: Moderate COPD

Stage 2

50% - 80% Normal Lung Function

COPD Stages III: Severe COPDCOPD Stage III typically involves severe

restraint of Respiration, tininess of breath and

frequently COPD exacerbations

Stage 3

30 – 50% Normal Lung Function

COPD Stages IV: Very Severe COPDCOPD Stage IV become very severe and risky

and thus decreases the life quality with vital

COPD Exacerbations.

Lung function FEV1 levels might lower that than

30%

Stage 4

Less than 30% Normal Lung Function

You admit a patient with AECOPD. What is the most

effective method to deliver rescue beta2 agonist (Albuterol)?

A. Metered dose inhaler (MDI)

B. Dry Powder Inhaler (DPI)

C. Soft Mist Inhaler (SMI)

D. Aerosol nebulizer

Classes of Inhaled Medications

Maintenance:

Long Acting Beta Agonists (LABA)

Improve lung function, reduces SOB, improves mucus

clearance

Long Acting Muscarinic Antagonists (LAMA)

Improve lung function, reduces SOB, reduces AECOPD

LABA/LAMA – new FDA approved

Quick relief:

Short Acting Beta Agonists SABA/SAMA

Reduces SOB/symptoms

Inhaled Medications

Inhaled Steroids:

Fluticasone/Salmeterol

Beclomethasone

Budesonide/Formoterol (Symbicort)

Budesonide

Bronchodilators:

Arformoterol (Brovana)

Ipratropium (Atrovent)

Tiotropium (Spiriva)

Levalbuterol (Xopenex)

Albuterol (AccuNeb)

Ipratropium bromide/Albuterol (DuoNeb)

Formoterol (Foradil)

Salmeterol Indacaterol(LABA)

LABA/LAMA Combo Bronchodilators

Medications: Type FDA Approved

Umeclidinium/vilanterol

(Anoro®/Ellipta® PI)

DPI 12/2013

Indacaterol/glycopyrronium bromide

(Utibron™/Neohaler® PI)

DPI 10/2015

Tiotropium bromide/olodaterol

(Stiolto™/Respimat®)

SMI 05/2015

Glycopyrrolate/formoterol fumarate

(Bevespi Aerosphere™PI)

pMDI 04/2016

Indications:High risk – severe or very severe airflow limitation;

> 2 AECOPD per year;

> 1 hospitalization for AECOPD

Treatment Modalities

Type Pros Cons

MDIs

Metered

Dose Inhalers

HFA driven

Breath actuated

Quick & easy to use

Independent of insp. flow

Low cost

Wide variety of meds

Coordination between

actuation & inspiration

May need spacer

High oropharyngeal deposition

DPIs

Dry Powder

Inhaler

Single dose

Multi dose

Power assisted

Some breath

actuated

Quick & easy to use

Does not require coordination

No spacer required

Inspiratory flow dependent

Poor dose reproducibility

Affected by humidity

SMIs

Soft Mist

Inhaler

Does not require coordination

No spacer required

Slow velocity aerosol

Dose loading into device

Only 1 company uses this

method - limited

Nebulizers Jet

Ultrasonic

Vibrating mesh

High patient adherence

Slow velocity aerosol

Bulky

Power source needed

Frequent cleaning

Bonini & Usmani COPD Research & Practice (2015); 1:1-9

64 year old female with SOB

Productive cough

She is extremely anxious

PMH: HTN, COPD Stage 3 (moderate 30 – 50% of

lung function), on home inhaled steroids & Spiriva

Lungs with diminished breath sounds, expiratory

wheezing

Not moving much air

O2 sats on 2 L NC 87%

Looks dusky

What would you like to do?

Case continued…

Get a chest x-ray

Give a Beta2 agonist – rescue strategy

How? MDI? Aerosol nebulizer?

Steroids

ABG

COPD Exacerbation Treatment

Bronchodilators – some thought to limited benefit

Short course of corticosteroids – 7 to 10 days

Methylprednisolone or Prednisone

No advantage of IV over PO

NNT = 10 (Steroids)

Case continued…

Give a Beta2 agonist – rescue strategy

How? MDI? Aerosol nebulizer?

Steroids

ABG

• HR 115, RR 26, labored with forced exhalation

• Accessory muscle usage noted

• Unable to complete a full sentence

• Receiving bronchodilators. Sats 86% on 5L NC

ABG: pH 7.36 PaCO2 48 PaO2 53 HCO3 28

The decision is to place the patient on non-invasive

ventilation. Which do you choose?

A. CPAP

B. Hi-Flow NC

C. BiPAP

ABG reminder:

ABG: pH 7.36, PaCO2 48, PaO2 53, HCO3 28

Hi-Flow NC, How Does It Work?

Blended air & oxygen produce a specific

FiO2 (0.21 - 1.0)

Flow rates between 20 LPM & 80 LPM

adjusted at specific FiO2

Higher flow rates wash out anatomical dead

space

May produce small amounts of PEEP

2 - 4 cm H20 pressure

What Hi-Flow does for COPD

Washes out dead space increasing alveolar minute

ventilation

Can decrease WOB

Heats and humidifies inhaled gas as well as the

natural airway can

PEEP??

What CPAP does for COPD

Decreases auto-PEEP

aka occult PEEP, inadvertent PEEP

Caused by incomplete exhalation of alveoli

Improves ventilation to perfusion matching

Decreases muscle work

Lessens CO2 production

Lessens O2 consumption

Buys “time” for some other intervention to work

Steroids

Bronchodilators

Non-Invasive Ventilation Challenges

Leaks in system can

effect how well it works

Mask size

Face shape

NG or feeding tubes

Facial hairThis Photo by Unknown Author is licensed under CC BY-NC-ND

Skin Breakdown in a relatively short period of time

Non-Invasive Ventilation Challenges

Gastric Distension

Esophageal sphincter opening pressure is

approximately 20 cm H20

Aspiration

May need NG tube

Use with caution in:

Gastric bypass

Gastric surgeries

Poor esophageal sphincter tone

When do you choose CPAP over BiPAP?

Hypoxic Respiratory Failure: CPAP good first option

Elevated RR

Low PaO2 or sats

Normal pH

Maintaining “normal” or low PaCO2 for patient

ABG: pH 7.40, PaCO2 48, PaO2 53, HCO3 28

*The patient was initially in hypoxic respiratory failure superimposed on chronic respiratory failure.

PaCO2 is lower than normal due to increased RR.

Case continued…

Patient is placed on CPAP

She is anxious, but calming down

Rests on CPAP for about an hour

Steroids given, couple of albuterol nebs

CXR likely bronchitis exacerbation

Now the patient is getting increasingly confused

What would you like to do?

Which rescue strategy would you like to use now for this

patient? An ABG reveals the following: pH 7.28/PaCO2 74/

PaO2 103/ HCO3 30.

A. More nebulizer treatments & steroids

B. Intubate & mechanically ventilate

C. CPAP of +5 cm H20

D. BiPAP +12 (IPAP), +8 (EPAP)

When do you choose BiPAP over CPAP?

Hypercarbic Respiratory failure: BiPap better option

Elevated RR

pH acidotic

High PaCO2

Usually accompanied by increased WOB

May also have low PaO2 – hypoxic failure

*He developed acute hyperbaric respiratory failure superimposed on chronic respiratory failure. Hypoxia is improving.

pH 7.33, PaCO2 58, PaO2 70, HCO3 28

Continuous Positive Airway Pressure (CPAP)

vs. Biphasic Positive Airway Pressure (Bi-PAP)

This Photo by Unknown Author is licensed under CC BY-NC

2 hours later the patient is becoming more somnolent, very

difficult to arouse.

His repeat ABG: pH 7.22/PaCO2 88/ PaO2 116/ HCO3 32.

A. Uncompensated metabolic acidosis

B. Partially compensated metabolic

alkalosis

C. Partially compensated respiratory

acidosis

D. Compensated respiratory alkalosis

Considering his repeat ABG, what

would you like to do?

A. Nebulizer treatment & steroids

B. Intubate & mechanically ventilate

C. CPAP of +5 cm H20

D. BiPAP +12 (IPAP), +8 (EPAP)

ABG reminder:

ABG: pH 7.22, PaCO2 88, PaO2 116, HCO3 32

Application:

The patient gets intubated

What considerations should you keep in mind when

determining ventilator settings?

Reminder ABG:

pH 7.22/PaCO2 88/ PaO2 116/ HCO3 32

Make sure he’s on steroids!

What initial ventilator settings would you like?

Options for initial vent settings for

AECOPD: pH 7.22/PaCO2 88/ PaO2 116/ HCO3 32

A. AC 560, 22, 100%, +10 PEEP

B. AC 560, 8, 50%, +10 PEEP

C. VC 700, 20, 50%, +5 PEEP

D. VC 700, 8, 70%, +5 PEEP

AC 560, Rate 8, 50%, +10 PEEP

Reminder ABG:

pH 7.22/PaCO2 88/ PaO2 116/ HCO3 32

Why these settings?

560 Vt is about 8 cc/kg PBW

Rate 8 – allows longer time in exhalation

50% - Patient is a bit hypoxic

+10 PEEP – will act as a stent for distal airways

Key points:

Don’t blow off the CO2 too quickly (increased rate)

Risks: ↑ Hyperinflation, air trapping, auto-PEEP

Goal should be a “reasonable” pH

COPD Exacerbation Treatment:

Antibiotics

Antibiotics are debated as

many infections are viral

Strep pneumonia

H. flu

Problem: antibiotic

resistance

Oxygen Therapy

Haldane effect disproven

General guideline:

Keep low 90%, avoid high concentration of O2

If O2 needed, monitor for signs of hypercapnia

Non-invasive ventilation

Intubate if:

-Respiratory distress with hemodynamic compromise

-Mental status change, somnolence

-Worsening acidosis

Monitor for intrinsic PEEP (auto-PEEP)

Reducing 30-Day Readmissions

Reduction of up to 3% of Medicare payment

Focused education on:

Inhaler use

Smoking cessation

Action plans

Assessment of:

Goals of care

Oxygen needs

Spirometry testing

Follow up plan including:

Phone call 48 – 72 hours post discharge

Follow up with provider in 7 – 10 days

Pulmonary Rehab

Home care services (if applicable)

Patient navigator

28 – 68% of patients don’t know how to use their MDI & DPI correctly.

Why? There’s 9 steps on average!

TORCH Study

6112 patients, observational study

79.8% “good” adherence

Taking at least 80% of prescribed inhaled meds

Good adherence =

↓ mortality (11.3% vs. 26.4%) &

↓ exacerbations (0.15/year vs. 0.27/year)

Other long term management:

Dyspnea management

Anxiety → bronchospasm → AECOPD

Diaphragmatic breathing techniques

Avoid respiratory infections

Flu & pneumococcal vaccines

When should nebulizers be used?

Elderly

Severe disease with frequent exacerbations

Physical &/or cognitive impairments

Structural changes in the brain?

60 outpatient (30 with COPD, 30 without – control)

COPD patients had regionally decreased gray matter volume in the anterior, mid, and posterior cingulate cortex, hippocampus, and amygdala

Areas that process dyspnea, fear, and antinociception

Levels of degeneration in certain areas of the brain were also impacted by longer disease duration

Those individuals showed a greater fear of breathlessness and fear of physical activity, which can affect the course of the disease

Roland W. Esser, Dipl-Psych; M. Cornelia Stoeckel, PhD; Anne Kirsten, MD; Henrik Watz, MD; Karin Taube, MD; Kirsten Lehmann; Sibylle

Petersen, PhD; Helgo Magnussen, MD; Andreas von Leupoldt, PhD Chest. 2016;149(2):426-434.

Other long term management:

QUIT SMOKING!!!

Pulmonary rehabilitation

Decreased readmissions

Diaphragmatic breathing techniques

Avoid respiratory infections

Flu & pneumococcal vaccines

Palliative care

Unveiling The Mysteries of Mechanical Ventilation

ARDS MANAGEMENT: A CASE BASED APPROACH

Objectives

Define ARDS using the Berlin Definition

Explore lung protective ventilation strategies

through a case based discussion

Identify refractory hypoxemia and evidence-based

rescue strategies

Case Study

52 year old male admitted with pneumonia 2 days ago and is now showing signs of sepsis.

PMH: HTN, otherwise healthy

Received 7 Liters of fluid & IV antibiotics since admission

Now on Telemetry Unit

Rapid Response initiated because feeling SOB with dropping SaO2

Now coming to your ICU on 100% NRB mask

What would you like to do?

Labs, ABG, chest x-ray

Lab results:

pH 7.22

PaCO2 68

PaO2 82

HCO3 20

SaO2 91%

Lactate 2.5 mmol/L

Na+ 134

K+ 3.8

Glucose 132

WBC 20.9

Neutrophils 19

Considering the patients labs & chest

x-ray, what would you like to do?

A. Try a nebulizer & steroids stat!

B. Place on high flow nasal cannula

C. Place on CPAP

D. Place on Bi-Pap

E. Intubate & mechanically ventilate

ARDS: What is it?

ARDS is a clinical syndrome of lung injury with

hypoxic respiratory failure caused by intense

pulmonary inflammation that develops after

a severe physiologic insult.

What was this patient’s insult?

Acute Respiratory Distress Syndrome (ARDS)

▪ Inflammatory lung disease

It is not a primary disease, but a result of:

▪ Sepsis

▪ Trauma

▪ Multiple blood transfusions (TRALI, CRALI)

▪ Pancreatitis

▪ Cardiopulmonary bypass

▪ Pulmonary contusion

▪ Pneumonia/aspiration

Inflammatory Response →

Physiologic Effects

❑ SIRS response and uncontrolled release of inflammatory mediators

❑ Vasodilation

❑ ↑ microvascular permeability

❑ Cellular activation adhesion

❑ Coagulation

❑ ARDS is the manifestation of “SIRS” in the lungs

❑ Can quickly lead to inflammation in other end organs

This Photo by Unknown Author is licensed under CC BY-SA

What is happening?

INFLAMMATORY RESPONSE!

Alveoli are infiltrated with

leukocytes

Fibrin deposits in lungs

Widespread endothelial &

alveolar damage

Leaky capillaries

Lungs get stiff

decreased compliance

Non-cardiogenic pulmonary

edema

Signs:

Tachypnea

Progressive refractory

hypoxemia

◼ (refractory to increases in

FiO2)

◼Worsening P/F ratio

◼ (PaO2 divided by FiO2)

CXR – Bilateral pulmonary

infiltrates

Usually require mechanical

ventilation within 48˚

PaO2/FiO2 Ratio or P/F ratio

Relationship of amount of additional oxygen to

create a specific PaO2

Formula: PaO2/FiO2

Normal is > 300

Our patient: PaO2 82/1.0 = P/F 82

Used to define levels of ARDS

ARDS: The Berlin Definition `

Gordon D. Rubenfeld, MD ,JAMA. 2012;307(23)

Berlin Criteria - 2012

ARDS Severity PaO2/FiO2* Mortality**

Mild 200 – 300 27%

Moderate 100 – 200 32%

Severe < 100 45%

*on PEEP 5+; **observed in cohort

Gordon D. Rubenfeld, JAMA. 2012;307(23)

Does our patient have ARDS?

Timing?

Yes, within 1 week

Chest x-ray?

Yes

Origin of edema?

No CV fluid overload

P/F ratio?

PaO2/FiO2

82/1.0 = 82 P/F ratio

Does this patient have ARDS?

A. Yes

B. No

This patient

now has

SEVERE ARDS

based on the

Berlin Definition

Case Study

Initial Vent Settings:

ABG : pH 7.22/PaCO2 68/PaO2 82/HCO3 20

Mode: Volume Control (VC+)

Tidal volume (Vt): where should we set it?

◼ Note: Patient weighs 90 kg, height 5’8”

◼ PBW (male, 5’8”: 547 – 8 cc/kg)

Rate: 18 (pick something – look at the PaCO2)

PEEP: +8

FiO2: 100% PaO2/FiO2

82/1.0 = 82

Predicted Body Weight Charts

Now What? Lung Protective Ventilation

Compared 6 mL/kg versus 12 mL/kg

Limited plateau pressures < 30 cm H2O

Reduction in mortality from 40% - 31% (9% reduction!)

More ventilator free days (12 days vs. 10 days)

ARDS Management Con’t

Low tidal volume

6 ml/kg

Allow permissive hypercapnia

PEEP:

Like a stent to keep the alveoli open

When increasing PEEP, monitor for signs of decreased cardiac output!!!

PEEP Ladder from ARDSNet

What therapy will improve the PaO2?

PEEP!

This Photo by Unknown Author is licensed under CC BY-NC

Concepts from the Trial that Continue

“Less is more” - limit tidal volumes to 4 – 6 ml/kg

PBW

Always base tidal volumes on PBW

Lower expectations for pH & PaO2

Keep pH > 7.15

How much PaCO2 is too much????

PaO2 goal > 55 mm Hg, but < 80 mm Hg

Concepts from the Trial that Continue

Use plateau pressures as a guide for when to

decrease tidal volume and lessen “volutrauma”

Target number is plateau pressure ≤ 30 cm H20

If plateau pressure > 30, decrease tidal volumes until

pressures < 30 and/or minimum volume of 4 cc/kg

reached

Use PEEP equally as much for “protection“ as you

do for oxygenation

In ARDs, minimize lung injury!

❖ Volutrauma:

❖ Alveoli & bronchioles damaged by

excessive levels of Vt

❖ Over-inflation of lungs which physically

damages the tissue

❖ Often the result of improper or

incorrect use of a medical ventilator

❖ Atelectrauma

❖ Lung injury caused by sheering forces

❖ Barotrauma

❖ Damage to the lung from rapid or

excessive pressure changes, such as high

airway pressures on the ventilator

This Photo by Unknown Author is licensed under CC BY-SA

Back to our case…

Started on LPV Vent settings:

VC 547 (8 cc/kg PBW)

RR 18

PEEP +8

FiO2 100%

Repeat ABG: pH 7.30/PaCO2 58/PaO2 74/HCO3

22

Peak Inspiratory Pressure: 54, Plateau Pressure: 42

Are the ventilator settings “Lung Protective”?

Next steps: pH 7.30/PaCO2 58/PaO2 74/HCO3 22

A. Decrease the PEEP, increase the tidal volume

B. Increase the PEEP, increase the tidal volume

C. Decrease the PEEP, decrease the tidal

volume

D. Increase the PEEP, decrease the tidal volume

E. Hold tight

F. Place on oscillatory ventilator

Assessing compliance “static”

pressure

What is it?

How to assess:

Vt / (plateau pressure – PEEP)

547 / (42 – 8) = 16

Normal compliance is > 50

Compliance should be calculated with ANY change in PEEP!!!! (up or down)

Are you happy with this patient’s compliance?

New vent settings:

Last ABG: pH 7.30/PaCO2 58/PaO2 74/HCO3 22

VC+ 479 (7 cc/kg PBW)

RR 20

PEEP +12 (Done gradually over 45 min)

FiO2 100%

Repeat ABG: pH 7.31/PaCO2 56/PaO2 86/HCO3

23

Peak Inspiratory Pressure: 58, Plateau Pressure: 38

Compliance: Vt / (plateau pressure – PEEP)

479 / (38 – 12) = 18 (was 16)

Next steps:

A. Decrease the PEEP, increase the tidal volume

B. Increase the PEEP, increase the tidal volume

C. Decrease the PEEP, decrease the tidal volume

D. Increase the PEEP, decrease the tidal volume

E. Hold tight

F. Place on oscillatory ventilator

New vent settings:

Last ABG: pH 7.31/PaCO2 56/PaO2 86/HCO3 23

VC+ 479 (6 cc/kg PBW)

RR 20

PEEP +16 (Done gradually over 30 min)

FiO2 100%

Repeat ABG: pH 7.29/PaCO2 54/PaO2 104/HCO3

24

Peak Inspiratory Pressure: 54, Plateau Pressure: 34

Compliance: Vt / (plateau pressure – PEEP)

410 / (34 – 16) = 18 (was 18)

Next steps:

A. Decrease the PEEP, increase the tidal volume

B. Increase the PEEP, increase the tidal volume

C. Decrease the PEEP, decrease the tidal volume

D. Increase the PEEP, decrease the tidal volume

E. Hold tight

F. Place on oscillatory ventilator

New vent settings:

Last ABG: pH 7.29/PaCO2 54/PaO2 104/HCO3 24

VC+ 342 (5 cc/kg PBW)

RR 22

PEEP +18

FiO2 100%

Repeat ABG: pH 7.28/PaCO2 52/PaO2 128/HCO3

24

Peak Inspiratory Pressure: 40, Plateau Pressure: 30

Compliance: Vt / (plateau pressure – PEEP)

342 / (30 – 18) = 28.5 (was 18)

Driving pressure theory….makes us

feel better about high PEEP

Driving pressure ( ∆P=Vt/Crs) identified as ventilation variable

most strongly associated with survival in this retrospective data

analysis.

Driving Pressure

Driving Pressure = the difference between plateau

pressure and PEEP

pPlat-PEEP

35 – 15 = 20 driving pressure

Number used to calculate compliance of the lung

◼ Cs= vt/plateau-PEEP

As PEEP is increased, if lung compliance improves in

theory so should mortality.

Graph A: PEEP stays the same but

plateau pressure rises, difference

gets bigger ( compliance

decreases): result increased

mortality

Graph B: Peep increases, Plateau

rises at same rate, no difference

between the two ( compliance

stays the same): result no change in

mortality

Graph C: PEEP increases, plateau

pressure stays the same but

difference between the two gets

smaller ( compliance improves):

decrease in mortality

Driving Pressure in Our Case

Repeat ABG:

pH 7.29/PaCO2 54/PaO2

104/HCO3 24

Peak Inspiratory Pressure:

54, Plateau Pressure: 34

Compliance: Vt / (plateau

pressure – PEEP)

410 / (34 – 16) = 23

Driving pressure:

34 – 16 = 18

Repeat ABG:

pH 7.28/PaCO2 52/

PaO2 128/HCO3 24

Peak Inspiratory

Pressure: 40, Plateau

Pressure: 30

Compliance: Vt /

(plateau pressure – PEEP)

342 / (30 – 18) = 28.5

Driving pressure

30 – 18 = 12

Refractory Hypoxemia

Working Definition:

PaO2 < 60 mm Hg on an FiO2 of 80-100% and

PEEP of > +10 for more than 12 - 24 hours

Manifests in severe ARDS

“Rescue strategies” typically deployed at this time

Adjuncts to standard care that have been shown to

have some benefit but not necessarily improve outcomes

or have little evidence to support it.

What Rescue Strategies work?

You Be the Judge!

ARDS Management

Should we be placing patients in the

prone position with ARDS?

A. Yes, there is definite benefit!

B. No, the evidence isn’t there.

Prone Positioning

• Changes the “zones” of ventilation

• Uses gravity to re-distribute fluids

• Can improve V/Q matching ( ventilation to perfusion)

• Takes pressure off of aorta

• May also take pressure of abdomen off of diaphragm and

chest wall

• Prospective, RCT

• 466 total patients with severe ARDS defined by P/F

ratio < 150 cm H20, PEEP at least 5, FiO2 at least .60,

and Vt close to 6cc/kg PBW

• 237 prone group and 229 in supine group

• Prone group left prone for at least 16 hours

• Outcome measure was all cause mortality within 28 days

after inclusion

N EnglJ Med2013;368:2159-68 DOI 10.1056/NEJMoa1214103

N EnglJ Med 2013;

368:2159-68

This Photo by Unknown Author is licensed under CC BY-NC

Are neuromuscular blockers beneficial for treating

patient with ventilator dysynchrony in the setting of

ARDS?

A. Yes, we should be using neuromuscular

blockade

B. Heck no! Don’t paralyze patients

C. The data isn’t clear

Neuromuscular blockade

Multicenter RCT of 340 patients with severe ARDS

Early use of 48 hours of neuromuscular blockade reduced mortality compared to placebo

NNT of 11 to prevent one death at 90 days in all patients, and a

NNT of 7 in a pre-specified analysis of patients with a P:F ratio <120.

Note: patients randomized to paralytic did not have an increased incidence of ICU-acquired weakness at 28 days.

Reference: Papazian L, Forel JM, Gacouin A, et al. for the ACURASYS Study Investigators. Neuromuscular blockers in early acute respiratory

distress syndrome. N Engl J Med 2010;363:1107-16.

PETAL Network

Clinical Trials Network for the Prevention & Early Treatment of Acute Lung Injury

Harborview Medical Center is 1 of 14 sites

Funded by National Heart, Lung & Blood Institute

Build on ARDSnet work

Goal: RCTs for ARDS

ROSE Trial:

Re-evaluation Of Systemic Early neuromuscular blockade

Are steroids are beneficial in the

management of ARDS?

A. Yes, use steroids, they totally help!

B. No, steroids are of no proven benefit

C. They are helpful in some patients

What’s the evidence?

RCT 180 patients with persistent ARDS (7 - 28 days after onset):

Methylprednisolone (daily dose 2 mg/kg x 14 days then 1 mg/kg x 7 days) vs.

Placebo

Hospital mortality & 180-day survival were comparable

BUT, patients enrolled ≥ 14 days after ARDS onset had increased 60-day mortality

35% Steroids vs. 8% placebo, p = .02

Steinberg KP, Hudson LD, Goodman RB, et al. Efficacy and safety of corticosteroids for persistent acute respiratory distress

syndrome. N Engl J Med 2006; 354:1671-84.

Is there evidence to support the use of inhaled

Pulmonary Vasodilators (iNO, Epo.) in ARDS?

A. Yes, there is definite benefit!

B. No, the evidence isn’t there.

Inhaled Pulmonary Vasodilators

NO - Nitric Oxide

NO is a substance naturally released within the linings

of the arterial walls that causes them to relax and

widen as a response to increased oxygen demands, as

seen when we run or lift weights.

iNO is an inhaled gas for ARDS/refractory hypoxemia

◼ Only vasodilates the areas that it comes in contact with , the

areas actually ventilating

◼ Decreased shunt in these areas

◼ Decreases pulmonary resistance

◼ Does not affect systemic hemodynamics because it is inhaled

Inhaled Pulmonary Vasodilators

Epoprostenol (aka Flolan, Veletri)

Primary pulmonary vasodilator

Traditionally given via IV

When nebulized and inhaled it stimulates the natural

production of NO and acts like iNO

◼ Only vasodilates areas it comes in contact with, ventilated

lung

◼ Improved shunt

◼ Decreases pulmonary vascular resistance around ventilated

areas of lung

◼ Given through vent

What's The Evidence

Neither have been shown to change mortality

Neither are reimbursed by insurance for refractory hypoxemia

Both may improve oxygenation in the short term “Band-Aid” until the patient improves

Markedly differing $$$ tags

◼iNO about $286.00/hr

◼Epoprostenol roughly $32.00/hr

Some evidence to suggest that iNO may be associated with an increased rate of acute kidney injury.

Is it better to be aggressive with PEEP

in Refractory Hypoxemia?

A. Yes!!! We need to recruit alveoli

B. NO! We may over distend alveoli

C. The evidence is beneficial for using high

levels of PEEP

High vs. Low PEEP

A NHLBI ARDSnet randomized trial comparing high

and low PEEP strategies in 549 patients with ALI or

ARDS

No significant difference in mortality, ventilator-free

days, ICU-free days, or organ failure-free days in

the two groups.

Reference: Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute

respiratory distress syndrome. N Engl J Med 2004;351:327-36.

Yes but....

A growing body of literature suggesting that

tailoring PEEP to patient physiology in specific cases

may improve outcomes with a trend towards a

decrease in mortality

Stiff chest wall conditions

Severe ARDS

Morbid obesity

•14 morbidly obese patients with BMI 50 or greater

•Compared Recruitment maneuvers with decremental PEEP settings using

esophageal balloons

•Documented physician chosen PEEP levels with levels required according to

esophageal balloon

•Measured end expiratory lung volumes, PF, compliance

Results:

• Average difference between MD targeted PEEP and esophageal balloon

suggested PEEP about 9cm H2O

• Recruitment maneuvers seemed to be successful but not necessarily superior

• Higher levels of PEEP did not have anticipated negative hemodynamic effects

Refernce: Pirrone,M.;Fisher,D., et al. Recruitment Maneuvers and Positive End-EpiratoryPressure Titraion in Morbidly Obese ICU Patients. CritCareMed 2016,Feb;44(2): 300-7

Is Airway Pressure Release Ventilation (APRV)

associated with improved outcomes in ARDS?

A. Yes, there is definite benefit!

B. No, the evidence isn’t there.

C. Possibly, more studies needed to definitively

determine the answer

Change to non-traditional types of

mechanical ventilation

APRV

2 levels of “CPAP”

Vent cycles between pressures at pre set times

Patient effort not met by inspiration

MUST be spontaneously breathing

Settings

P high

◼ Highest pressure seen

P low

◼ Lowest pressure seen

T high

◼ How long in high pressure

T low

◼ How long in low pressureThis Photo by Unknown Author is licensed under CC BY-NC

APRV Literature

Currently, no randomized controlled or well powered studies

1 head to head LPV study

17 total patients randomized to either low volume ventilation or APRV

• Both arms protocolized

• Inclusion criteria: • Intubated < 36 hours

• P/F ratio <300

• bilateral multifocal infiltrates

• Outcome measure: Fewer ventilator free days

AM J Respir Crit Care Med 2010;181:A1691

APRV vs. ARDSnet Results

No clinically or statistically significant difference

between ventilator free days or ICU days

Limitations to study were very small sample size

Conclusion: APRV is not inferior to ARDSnet

ventilation strategy

AM J Respir Crit Care Med 181;2010:A1691

Does High Frequency Oscillatory Ventilation

(HFOV) improve survival in ARDS?

A. Yes, there is definite benefit!

B. No, the evidence isn’t there.

Literature

2 Randomized controlled trials looking at oscillation

as a first line defense for ARDS

Oscillate

Oscar

Neither trial demonstrated an improvement

Oscillate trial was a head to head comparison of

standard ARDSnet LPV vs. Oscillation

Stopped mid term at 800+ patients due to increased

mortality in Oscillation arm > 40%

OSCILLATE Trial

High Frequency Oscillation: no mortality benefit from HFOV being applied early in moderate and severe ARDS.

OSCILLATE found an increased mortality rate in the treatment group.

This was in the setting of a higher average mean airway pressure and increased vasopressor use.

These findings were in contrast to the results of a meta-analysis suggesting mortality benefit.

Note: this was not a study of HFOV as a salvage maneuver, but as a primary mode in ARDS.

Ferguson, ND, Cook, DJ, Guyatt GH et al. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med.

2013;368:795-805. OSCILLATE.

Young D, Lamb SE, Shah S, et al. High-Frequency Oscillation for Acute Respiratory Distress Syndrome. N Engl J Med. 2013;368:806-

13. OSCAR.

Use adjuncts to traditional or non-

traditional ventilation

High frequency percussive ventilation (HFPV)

Primarily used as a treatment & adjunct to standard

mechanical ventilation for secretion management

Very small studies suggesting it can be used as a

ventilation strategy with improved oxygenation in

patients with severe ARDS

Studies are limited, small sample size, only looking at

oxygenation outcomes not mortality

Should we consider ECMO in a patient with

refractory hypoxemia with ARDS?

A. Yes, there has been some benefit in

the literature!

B. No, the evidence isn’t there.

ECMO

This Photo by Unknown Author is licensed

under CC BY-NC-SA

This Photo by Unknown Author is licensed under

CC BY-NC-SA

VA-ECMOVV-ECMO

What's the evidence?

Highlighting both regionalization of care and use of ECMO, this trial showed that:

Transfer to an ECMO-ready facility (75% of those transferred actually received ECMO) led to:

NNT of 6 to prevent one death or severe disability at six months compared to standard care.

The study was limited by the lack of a mandated lung-protective strategy in the control group;

93% of those transferred for possible ECMO received a lung-protective strategy, compared to 70% in the control group.

Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal

membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet 2009;374:1351-63.

Should we run patients wet, euvolemic or dry

in the recovery phase?

A. A little extra fluid won’t hurt!

B. Euvolemic is where they need to be!

C. Dry to the bone!

What’s the evidence?

FACTT Trial, 1000 patients over 7 days with ALI

RCT compared:

Conservative fluid management using a complex protocol to a

Liberal fluid approach

Although there was no significant difference in the primary outcome of 60-day mortality, the conservative strategy of fluid management shortened the duration of mechanical ventilation and ICU stay without increasing nonpulmonary-organ failure.

Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med.

2006; 354:2564-75.

Back to our case…

Kept the patient on 4 – 5 cc/kg for 6 days, now increasing the tidal volume

Allowed the lungs to “rest”

What rescue strategies should we use?

Prone (> 16 hours per day)

Propofol for sedation, Fentanyl pushes prn

Vecuronium (total of 2 days)

Minimize fluid administration & did not overload ◼ Required Dobutamine for O2 delivery

Epoprostenol

◼ Vasodilate the portions of the lung that were actually being ventilated

◼ Increase V/Q matching in the ventilated lung segments

Day 8 - vent settings:

VC+ 547 (8 cc/kg PBW)

RR 22

PEEP +10

FiO2 50%

Latest ABG: pH 7.49/PaCO2 32/PaO2 182/HCO3 26

Peak Inspiratory Pressure: 40, Plateau Pressure: 24

Compliance: Vt / (plateau pressure – PEEP)

547 / (24 – 10) = 39 (was 28.5)

Want to make any changes?

Next day (Day 9)

VC+ 547 (8 cc/kg PBW)

RR 18

PEEP +8

FiO2 50%

Latest ABG: pH 7.46/PaCO2 38/PaO2 212/HCO3 28

Peak Inspiratory Pressure: 32, Plateau Pressure: 22

Compliance: Vt / (plateau pressure – PEEP)

547 / (24 – 8) = 34 (was 39)

P/F ratio: 424

Want to make any changes?

What would you like to do?pH 7.46/PaCO2 38/PaO2 212/HCO3 28, PIP 32, PP 22,

Compliance 34

A. Decrease rate, decrease the PEEP

B. SAT/SBT

C. Hold tight! No changes are needed!

D. Decrease the PEEP, increase the Vt

The RT comes to you in the am & states your patient failed

his SBT. The Propofol was still running.

What would be your best response?

A. OK (Thinking “awesome, I might get a break

today!”)

B. Ask the RT to come back & repeat the SBT

once the Propofol is off & the patient is awake

C. Decrease the Propofol & re-evaluate in the

afternoon

SAT & SBT

The Propofol is turned off and within 20 min the

patient is awake, but very anxious & restless

The patient keeps trying to tell you something, but

you have no idea

Given the last 9 days of the hospital stay, what are

you assessing during the SAT/SBT?

Thoughts…

Pain?

Orientation?

Delirium?

Secretion management

Overall strength

How fast is the patient

breathing?

What are the tidal

volumes?

Signs of distress?

What is their PO4

level?

Other electrolytes?

Spontaneous Breathing Trials (SBT)

Gold standard and well supported in literature

Everyone that qualifies should get one

Must be combine with an organize reduction in sedation

in order to be successful

Most effective when protocolized and not physician

driven

Spontaneous Breathing Trials

Basic criteria to do SBT:

Signs of reversal of process that got patient intubated

VE < 10 LPM

FiO2 ≤ .50

PEEP ≤ 8 cm H2O

Hemodynamically stable, can still be on pressor

Not paralyzed

Newly published ATS guidelines recommend SBT

done on +5 - 8 PS (2017)Reference: Ouellette,D.R., Patel,S. Et al. Liberation From Mechanical Ventilation in Critically Ill Adults: An Official American College of Chest Physicians/American Thoracic

Society Clinical Practice Guideline. Chest 2017; 151 (1):166-180

Spontaneous Breathing Trials

Trial should last minimum 30 minutes, no longer than 2 hours

ABG or other non-invasive measure in conjunction with clinical appearance used to assess tolerance

EtCO2

SpO2

Clinical signs of intolerance:

Increased WOB

Agitation

Diaphoresis

Increased VE

Desaturation

Apnea

Hemodynamic instability

Change in HR > or < 20% of baseline

Subjective “sense of doom”

You initiate a SBT on your patient. Their baseline EtCO2 is

38 mmHg. After 30 min the EtCO2 is 52 mmHg. How

would you interpret this?

A. This is great! Let’s extubate the patient!

B. It’s OK, but let’s go a little longer.

C. Suction the patient asap!

D. Boo, this patient is not ready for extubation.

What may be preventing this patient

from being liberated?

Pneumonia – secretions

Sick, inflamed lungs

Delirium

Pain/anxiety

Ventilator acquired weakness

Let’s get them off the ventilator!

Respiratory Care;June 2013, Volume 58, No. 6.

Weaning requires

balancing patient

demands with patient

capabilities.

When capabilities meet

demands, patients can be

removed from mechanical

ventilation.

A patient recovering from sepsis with a complication of a PE

fails an attempt to wean, would this be a failure likely due to

increased demand or strength capability?

A. Demand

B. Strength Capability

What happens if they fail?

Patients that fail should be returned to a level of

support that is restful

Try again another day

Later in the day if appropriate

If patients fail multiple days of attempts they can

be considered a long term wean

Short Term vs. Long Term Weaning

Most patients!

Post-op

Post pneumonia

Most ARDS

Post resuscitation

And many more

Failed multiple previous

weaning attempts

Underlying

neuromuscular conditions

Spinal chord injury

Severely malnourished

& deconditioned

Short Term Weaning Long Term Weaning

Long term weaning

Address why patient

may be failing

Demands too high

◼Fever

◼Metabolic issues

◼Sepsis

◼Burns

◼Head injuries

◼Unbalanced

nutrition

Mechanics

inadequate◼ Underlying muscle weakness

due to protracted illness

◼ Spinal chord injury

◼ Muscle weakness due to

disease process

◼ Guillen’ barre

◼ Myasthenia Gravis

◼ Deadspace too high

◼ Shunt too high

◼ Process that got them

intubated not quite resolved

VAE-Ventilator associated events

Delirium

PAD Guidelines – new guidelines coming this year!

Supplemental Information

New Proposed CMS Core Measure

(suspected will replace VAP tracking)

Ventilator Associated Event (VAE)

Not yet a core measure but literature is emerging

regarding identification and recommendations

All recommendations point to standardizing

evidence based practices regarding patients on

mechanical ventilators

VAE: Ventilator Associated Events

CDC Definition - 3-Tiered

Tier 1 – Ventilator Associated Condition (VAC)

Hypoxemia more than 2 days with escalating FiO2 and or PEEP settings

Tier 2 – Infection-related VAC (IVAC)

Hypoxemia in the setting of generalized infection or inflammation

Antibiotics instituted for a minimum of 4 days

Tier 3 – Probable ventilator-associated pneumonia (VAP)

WBC present on sputum gram stain

OR, pathogen

2013 PAD GUIDELINES

Pain

Treat pain first!!!

Ask the right questions

Do not use sedation to

treat pain

Pre-emptive pain plan

Treatments

Mobility

Behavioral pain

assessment scale (i.e.

FLACC)

Guidelines for special

populations:

Rib fractures

Abdominal aortic

aneurysm repair

Neuropathic pain

Critical Care Medicine January 2013

2013 PAD GUIDELINES

Agitation Minimize sedation Minimize & avoid benzo’s

Unless ETOH withdrawal Consider non-

benzodiazepines◼ Propofol◼ Dexmetomidine

Don’t overuse sedation “Light” sedation Avoid “deep” sedation

unless absolutely clinically warranted

Daily interruption Follow RASS with goal Consider non-pharmacologic interventions

General prevention considerations:

Glasses Hearing aids Day/night orientation Method of communicating if

barrier Reorientation frequently Board in room with place &

date Clock in view Noise control Promote sleep Cluster care activities***Daily checklists to

address PAD***Critical Care Medicine January 2013

META-ANALYSIS BENZO VS. NON-BENZO

2013 PAD GUIDELINES

Delirium Monitor for it!!! Prevent it!!!

Identify who is at risk Hand-offs Was the patient ever CAM positive? Current CAM?

If the patient develops delirium:

Identify reversible causes

Avoid benzo’sDexmedetomidine

(Precedex) associated with lower delirium risk vs. benzo

Review their medication list

Pharmacy

Critical Care Medicine January 2013

CAM-ICU

• Baseline changes +

• Inattention +

• LOC OR

• Disorganized Thinking

RICHMOND AGITATION SEDATION

SCALE (RASS)

RASS goal for most patients -1 to 0

MEDICATIONS – AVOID BENZOS IN

DELIRIUM!

Haloperidol Antipsychotic Monitor extrapyramidal effects

Muscle rigidity, akathisia, parkinsonism

Monitor QTc Caution with

hypokalemia Caution with Amiodorone

Hypotension Orthostatic – worse with

IV dosing Metabolized/eliminated by the liver

Quetiapine (Seroquel) Antipsychotic with sedative properties Monitor for common side effects:

Dry mouth, dizziness, headache, somnolence (anticholinergic)

Increased HR, BP, constipation, increased liver enzymes

Prolonged QTc (rare)

Note: these are off label use!!!

POST-ICU CARE SYNDROME “PICS”

Patient or family

Mental health

PTSD

Anxiety

Depression

Cognitive

Executive function

Memory

Attention

Physical

Pulmonary reserve

Neuromuscular

weakness

Does the care in the ICU matter long term?

10% of ICU patients are at risk

of developing long term PTSD

Mayur B. Patel, James C. Jackson, Alessandro Morandi, et al. Incidence and Risk Factors for ICU-related Posttraumatic Stress Disorder In

Veterans and Civilians. American Journal of Respiratory and Critical Care Medicine, 2016

Common symptoms:

Nightmares, breathlessness, communication

barriers, fear of imminent death

WHAT IS THE ABCDEF PROTOCOL?

Awakening & Breathing

Coordination

Delirium Identification &

Management

Early Exercise and Mobility

ABC

D

E

www.icudelirium.org

Intervention (SAT) group = More unplanned

extubation, but not more reintubations

P = 0.02

P = 0.01

Discharged from hospital sooner Better survival at 1 yr

Aliv

e

P = 0.04

Girard et al. Lancet 2008; 371:126-34

ABC“SAT + SBT” WAS SUPERIOR TO

CONVENTIONAL SEDATION + SBT

Safety Screens

Wake Up Safety Screen

No active seizures

No active alcohol withdrawal

No active agitation

No active paralytic use

No myocardial ischemia (24h)

Normal intracranial pressure

Breathe Safety Screen

No active agitation

Oxygen saturation >88%

FiO2 < 50%

PEEP < 7.5 cm H2O

No active myocardial ischemia (24h)

No significant vasopressor use

Girard et al. Lancet 2008; 371:126-34. Kress et al. Crit Care Med 2004; 32(6):1272-6Ely et al. NEJM 1996; 335:184-9

ABC

Stop & THINK

Do any meds need to be stopped or lowered?

Especially consider sedatives

Is patient on minimal amount necessary?

Daily sedation cessation

Targeted sedation plan

Assess target daily

Do sedatives need to be changed?

Remember to assess for pain!

Toxic Situations• CHF, shock, dehydration

• New organ failure (liver/kidney)

Hypoxemia

Infection/sepsis (nosocomial)

Immobilization

Non-pharmacologic interventions• Hearing aids, glasses, reorient,

sleep protocols, music, noise control,

ambulation

K+ or electrolyte problems

D

Don’t get delirious,

take sleep serious!

Early Exercise in the ICU

Early exercise = progressive mobility

Study design: paired SAT/SBT protocol with PT/OT from

earliest days of mechanical ventilation

Schweickert WD, et al. Lancet. 2009;373:1874-1882.

Wake Up, Breathe, and Move

E

Early Exercise Study Results

OutcomeIntervention

(n=49)Control(n=50) P

Functionally independent at discharge 29 (59%) 19 (35%) 0.02

ICU delirium (days) 2.0 (0.0-6.0) 4.0 (2.0-7.0) 0.03

Time in ICU with delirium (%) 33 (0-58) 57 (33-69) 0.02

Hospital delirium (days) 2.0 (0.0-6.0) 4.0 (2.0-8.0) 0.02

Hospital days with delirium (%) 28 (26) 41 (27) 0.01

Barthel index score at discharge 75 (7.5-95) 55 (0-85) 0.05

ICU-acquired paresis at discharge 15 (31%) 27 (49%) 0.09

Ventilator-free days 23.5 (7.4-25.6) 21.1 (0.0-23.8) 0.05

Length of stay in ICU (days) 5.9 (4.5-13.2) 7.9 (6.1-12.9) 0.08

Length of stay in hospital (days) 13.5 (8.0-23.1) 12.9 (8.9-19.8) 0.93

Hospital mortality 9 (18%) 14 (25%) 0.53

Schweickert WD, et al. Lancet. 2009;373:1874-1882.

E

PERFORM SAFETY SCREEN 1st

Patient responds to verbal stimulation (i.e., RASS > -3)

FiO2 < 0.6

PEEP < 10 cmH2O

No dose of any vasopressor infusion for at least 2 hours

No evidence of active myocardial ischemia (24 hrs)

No arrhythmia requiring the administration of new antiarrhythmic agent (24hrs)

If patient passes Exercise/Mobility Safety Screen, move on to Exercise and Mobility Therapy

If patient fails, s/he is too critically ill to tolerate exercise/mobility

E

Early Exercise & Mobility

Levels of Therapy*

1. Active range of motion in bed and sitting position in bed

2. Dangling

3. Transfer to chair (active), includes standing without marching in place

4. Ambulation (marching in place, walking in room or hall)

*All may be done with assistance.

E

Family Engagement

Empower the family

Include them as part of the team

F

VAE (VAP) Prevention

HOB elevation (30 – 45 degrees)

Mouth/endotracheal tube care (oral w/chlorhexidine)

Lung Protective Ventilator (LPV) strategies if ARDS

Early discontinuation of ventilator

Appropriate analgesia & sedation (avoid benzos)

Daily interruption of sedation

Early mobilization with or without ambulation

DVT Prophylaxis

GI Prophylaxis (caution!)

Balanced IV fluid administration

Common Bundle Strategies Not Well

Supported By the Evidence

May decrease incidence of VAP, do not effect

incidence of VAE

Oral care with chlorhexidine

◼ No decrease in vent days or ICU length of stay

◼ Did effect decrease of VAP likely secondary to decrease in

oral secretions and/or colonization of the mouth

Subglottic secretion drainage

◼ Significant reduction in VAP

◼ No change in ventilator free days, VAE , or ICU days

American Journal of Respiratory and Critical Care Medicine Volume 192 Number 12/ December 15

The evidence to support GI Prophylaxis?

Microsimulation model using literature derived

estimates of risks of using PPIs in UGIB vs. incidence

of HAP & CDI in medical patients

Initiation of PPIs were associated with increased

hospital risk of death

Higher risk for pneumonia & Cdiff infections

Unless the patient was on PPIs pre-hospital or UGIB,

stop giving PPIs!

Especially in non-ICU patients

Pappas, Jolly & Vijan (2016) Journal of Internal Medicine; 31(4)364-71.

Take home points…

ARDS is a process of inflammation in the lung that can lead to inflammation in other organs

Over-ventilation & cyclical injury of alveoli hasten this inflammatory process

Lung protective ventilation is the gold standard for ARDS

4 – 6 cc/kg PBW

Lower expectations for ABG’s don’t target “normals”

◼ pH > 7.20

◼ PaO2 > 55, < 80

◼ PaCO2 - not as concerned

Take home points…

Lung compliance matters!!!!

Follow lung compliance

◼Vt / (plateau pressure – peep)

◼ Lower the number the stiffer the lungs

◼The stiffer the lungs, the worse the outcome

◼PEEP can markedly improve compliance

◼PEEP can also counteract a stiff chest wall

◼DON’T BE AFRAID OF PEEP!!!!

Take home points…

Know when you have refractory hypoxemia

Use rescue measures for refractory hypoxemia

Listed in order of highest to lowest levels of evidence

◼ Paralytics

◼ Prone

◼ Physiological setting of PEEP

◼ Non-conventional ventilation

◼ APRV

◼ Percussive

◼ Oscillation

◼ ECMO

◼ Inhaled vasodilators