unveiling the mysteries of mechanical ventilation...since 2011 karen has been involved with both...
TRANSCRIPT
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
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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