Pulmonary In-service Bassem Srour, MD, FCCP. Pulmonary, Critical - - PowerPoint PPT Presentation

Pulmonary In-service

Bassem Srour, MD, FCCP. Pulmonary, Critical Care & Sleep Medicine. Jameson Health System.

To Go over list

• 1. Respiratory rate.
• 2. Pulmonary myths and Science.
• 3. Oxygen.
• 4. ABGs, Acid base disturbances.
• 5. Nebulizers.
• 6. CPAP/BIPAP.

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Respiratory Rate.

• 1. What is Normal ?
• 2. What dictates how fast we should breath.
• 3. Why should we care ?
• 4. What does it tell us about the patient?

3

What is Normal ?? Small Hint NOT 20

4

Respiratory Rate.

 CO2 dictates our Minute ventilation as the

PH needs to be maintained at around 7.40 Our body have 2 ways to buffer acids:

 HCO3 that takes days for kidney to make

more or get rid off

 Changing our CO2. That takes minutes.

5

Respiratory Rate.

 Minute Ventilation = RR x Tidal Volume.  Normal MV 6 L ± 2 L.  Tidal volume is affected by many variables

such as Weight, Height, muscle weakness...

 Normal VT is around 500cc for 70 kg male.  5 Ft obese elderly F with Kyphosis 300cc.  6” 5’ young Male Athlete 900cc.

6

Respiratory Rate.

 VT 900 cc x RR 10 = 9L MV  VT 300 cc x RR 30 = 9L MV  They are both Ventilating the same.  As we grow our lungs get bigger and our

Vt gets larger so our RR go down.

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Textbook Normal !!!

8

What about not perfectly healthy patients

9

So what is Normal ??

 A single value is of little clinical importance

unless its in the extremes. (RR 5 or 40)

 A trend is far more Valuable such as a

patient has been breathing at 10-16 and now is breathing at 26 something has changed.

10

We measure the saturation isn't that the same thing?

 No The lung has 2 functions oxygenate and

• ventilate. They are not related.

 Patient with one lung after pneumonectomy

could have a saturation near 100% but around double the normal respiratory rate. We need only about half a lung to maintain a “normal” Sat.

11

Why Should we care !!!

• 1. Any changes in the lung such as worsening

pneumonia or CHF will lead to an increase dead space leads to increase in the minute ventilation and respiratory rate to maintain the same PCO2 and blood PH.

• 2. Any patient that turns septic will have

more lactic acid and will have a higher respiratory rate to buffer the acidosis

12

Why Should we care !!!

 Respiratory rate is a VITAL sign because its

an early predictor of VITAL changes in the patient physiology and when early interventions are done the complications and bad patient outcomes can be avoided.

 The reason why the patients are not treated

home is to be observed for these complications !!!

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BREATHING MYTHS & FACTS

14

Myths #1 Breathing is regulated by need for oxygen

 Breathing is regulated by the CO2

concentration in the arterial blood and the

• brain. Whatever we do (sit, walk, eat, run,

sleep, etc.), CO2 concentration is kept within a narrow range (0.1% accuracy) by the breathing centre located in the medulla

• blongata of the brain

15

Myth #2 CO2 is a poisonous or toxic waste gas and a waste product to get rid off.

 CO2 is a powerful

vasodilator and regulates blood and

• xygen supply to the

brain, heart and all

• ther vital organs.

 Another CO2 effect is to

regulate the release of

• xygen by the blood in

the tissues.

16

Myth #3 More breathing means better body

• xygenation

 Hyperventilation REDUCES oxygen

supply to the brain, heart, liver, kidneys, and all other vital organs due to low CO2 induced vasoconstriction.

 “Take a deep breath, get more oxygen”, or

“Breathe deeper for better oxygenation” is nothing more than a myth.

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Myth #3 More breathing means better body

• xygenation

 That’s why the recommended ACLS Bag

rate in arrest in 10-12 / min.

 Hyperventilating a cardiac arrest patient

will worsen his vital tissues blood supply and cause worse gastric distention and increase the chance of aspiration.

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Myth #3 More breathing means better body

• xygenation

 Applying PEEP valve on the bag mask is

the right way to increase the saturation if needed in an intubation.

 Synchronizing bagging and patient

spontaneous ventilation is another way

Myth # 4 Oxygen is good for you

 “All chronic pain, suffering and diseases

are caused from a lack of oxygen at the cell level."

• Prof. A.C. Guyton, MD.

 It was thought to be the cause of all

illnesses so giving it to patients was the treatment of all diseases !!!

20

Oxygen

 Name derives from the Greek roots (oxys)

("acid", literally "sharp") and (gοnos) ("producer").

 The acid producing gas was never intended

to be part of the Tender, Love and care.

21

Oxygen toxicity

 Pulmonary toxicity occurs with exposure to

concentrations of oxygen greater 50%.

 Signs of pulmonary toxicity begins with

evidence of tracheobronchitis, or inflammation of the upper airways, after an asymptomatic period between 4 and 22h.

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Oxygen toxicity

 Lead to decline in lung function as quickly

as 24h of continuous exposure to 100%

• xygen, with evidence of diffuse alveolar

damage and the onset of ARDS usually

• ccurring after 48 h on 100%.

 Breathing high concentration of oxygen

also leads to collapse of the alveoli (Atelectasis).

23

So what's the worse that can happen with giving too much

• xygen to a patient as long as

its less than 50%.

Hyper - oxygenating a patient will make us loose the ability to detect early physiologic changes.

24

Example

 Patient Sat is 98 % on RA and was placed

• n 4L NC in the ER. We kept it the same

and his Sat now is 99%.

 Patient has worsening CHF from a silent MI

• r worsening pneumonia on poor antibiotics
• selection. By the time he desaturates on 4L
• xygen the condition is much worse and we

might be too late to intervene and prevent intubation.

25

Who think this is a problem?

 Combine this practice:

1.

Not accurately documenting RR over 30 S

2.

Giving oxygen while the Sat on RA >90%

3.

Titrating oxygen up without investigating what caused it and what can we do to prevent the future worsening. NEXT Rapid response, intubation or arrest !!

ABGs

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ABGs Made simple

 Its useful in assessing Acid/base status.  Measure the PCO2 level.  Determine the PO2 and the A-a Gradient.  Not needed for oxygenation in general as

pulse ox saturation is very accurate if we have a good pulse wave.

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ABGs Made simple

 PH 7.4 (7.35 – 7.45) in normal.  > 7.45 Alkalosis.  <7.35 Acidosis.  PCO2: 40 mmhg ( 35 – 45) normal.  HCO3 on ABG is calculated and CO2 on

BMP is measured and its more accurate. 24 (22 -26 ) normal. PCO2 and CO2 (Bicarb) are not the same

29

ABGs Made simple

 PCO2 is Lung/CNS problem.  HCO3 is kidney/GI/Perfusion problem.  Condition is either too much or too low.  Usually it’s a combination and a

compensatory mechanism.

 The condition can also be acute or chronic.

30

Is it Respiratory or Metabolic?

1.

Respiratory Acidosis

2.

Respiratory Alkalosis

3.

Metabolic Acidosis

4.

Metabolic Alkalosis



Increased pCO2 >45



Decreased pCO2<35



Decreased HCO3 <20



Increased HCO3 >28

Common Conditions

 Metabolic Acidosis:

PH HCO3 PCO2

• 1. Septic shock with high lactic acid.
• 2. Ingestion of an external acid like anti freeze
• 3. Diabetic Keto-acidosis
• 4. Diarrhea and loss of GI Bicarb.
• 5. Renal failure cause lack of production of

bicarb and no clearing acids by the kidneys.

32

Common Conditions

Respiratory Acidosis:

 Acute: PH, N HCO3, PCO2.  Chronic: PH, HCO3, PCO2.

The Kidney needs time to make changes and get increase the HCO3 to try to get the PH as close to 7.4 as possible.

33

Common Conditions

 Common causes for Acute Resp Acidosis:

Acute drug overdose that suppress respiratory drive such as Benzo and opiates. Acute COPD, Asthma attack.

 Common causes for Chronic Resp Acidosis:

Chronic advance COPD, Severe Muscular weakness, Severe Kyphosis, Untreated OSA

34

Common Conditions

 Metabolic alkalosis: PH HCO3 PCO2

• 1. Vomiting and loss of gastric acids
• 2. Excessive NG suctioning and loss of gastric

acids

• 3. External ingestion of large amounts of

alkaline antacids.

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Common Conditions

Respiratory Alkalosis :

1.

Acute: PH, N HCO3, PCO2.

2.

Chronic: PH, HCO3, PCO2. The Kidney needs time to make changes and get rid off the HCO3 to try to get the PH as close to 7.4 as possible.

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Common Conditions

 Common causes for Acute Resp Alk:

Pain, Anxiety, Psychosis, Sepsis, PE, Asthma, Pneumonia.

 Common causes for Chronic Resp Alk:

Progesterone during pregnancy. Toxins in patients of chronic liver disease.

37

Bronchodilators

Not part of our Tender, Love and Care. They are not Harmless.

Bronchodilators

1.

They can worsen the patient oxygenation.

2.

Linked to a worse ARDS mortality.

3.

Prolong the time on ventilator in ARDS.

4.

They can induce tachyarrhythmia's.

5.

They can induce ischemia in CAD Pts. USE ONLY WHEN INDICATED !!!!

39

Bronchodilators

 BALTI-2 and ALTA large studies.

Both showed detrimental effects of the use

• f B agonist in patients with ARDS/ALI.

They are indicated to treat Bronchospasm not lung disease.

40

Bronchodilators

 The lung has selective Vasoconstriction and

• ventilation. When part of the lung is

working poorly the blood and the air is shifted to the “good” parts of the lung.

 Bronchodilators can shift air to non

perfused “bad lung” and thus worsen the

• xygenation of the patient.

41

Non Invasive Ventilation

NIV CPAP / BIPAP

Non invasive ventilation

1.

What's the difference?

2.

Why do we use one over the other?

3.

Clinical Benefits of NIV

4.

Indication of success or failure

5.

Possible abuse complications

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Differences

 CPAP: Continuous one pressure,

Best for OSA and CHF.

 BIPAP: Alternating between EPAP/IPAP.

Best for respiratory failure and hypercapnia We can set a respiratory back up rate.

44

CPAP

• 1. It does not increase tidal volume nor does

it support the patient’s minute ventilation.

• 2. In OSA it splints the oropharynx open.
• 3. It improves oxygenation for patients with

acute CHF by recruiting alveoli, decreasing the work of breathing, decreasing venous return and improving cardiac out put by as much as 50%.

BIPAP = PEEP + PS

EPAP has the same benefits as CPAP or PEEP on a ventilator. IPAP is similar to pressure support on

• ventilator. The difference between EPAP

and IPAP dictates the Pressure support and the amount of increase in a patient minute ventilation.

BIPAP

 BIPAP 5/10: PEEP 5, PS 5.  BIPAP 10/15: PEEP 10, PS 5.  BIPAP 5/15 or 10/20 have the same PS of

10 and thus will support the minute ventilation the same way.



EPAP for O2 and PS for CO2

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Benefits in Acute Care

Reduces need for intubation Reduces incidence of nosocomial pneumonia Shortens stay in intensive care unit Shortens hospital stay Reduces mortality Preserves airway defenses Improves patient comfort Reduces need for sedation

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Clinical scenarios for use

• 1. Acute exacerbation of COPD
• 2. Acute asthma
• 3. Hypoxemic respiratory failure
• 4. Community acquired pneumonia
• 5. Cardiogenic pulmonary edema
• 6. Immunocompromised patients
• 7. Postoperative patients
• 8. Postextubation failure
• 9. DNI status

Indicators of success in NPPV use

• 1. Young age
• 2. Less sick patients
• 3. Able to cooperate
• 4. Moderate hypercapnia PCO2 (45-90)
• 5. Moderate acidosis PH ( 7.35 - 7.10 )
• 6. Improvement of ABG, RR, HR in 2h

Criteria for Terminating NIV and intubation

• 1. Worsening pH and PaCO2
• 2. RR > 30 breaths/min
• 3. Hemodynamic instability
• 4. Oxygen saturation < 90%
• 5. Decreased level of consciousness
• 6. Inability to clear secretions
• 7. Inability to tolerate interface

Contraindications to NPPV

• 1. Cardiac arrest
• 2. Non respiratory organ failure
• 3. Severe encephalopathy
• 4. Severe upper GI bleeding
• 5. Hemodynamic instability
• 6. Unstable cardiac arrhythmia
• 7. Facial deformity or fascial trauma.

Contraindications to NPPV

1.

Upper airway obstruction

2.

Inability to cooperate

3.

Inability to protect the airway

4.

Inability to clear secretions

5.

High risk for aspiration

6.

Untreated pneumothorax

7.

Unstable respiratory drive.

Worst case scenario with NIV

 Use while contraindicated or failing to

recognize that the trial is not effective early in the course of the disease will increase the chance for crash intubation or cardiac arrest.

 Delay in intubation will lead to much higher

chance of aspiration pneumonia and worse patient prognosis.

Education

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Experience based professions

Experience Time

Knowledge based professions

knowledge Time

GOAL

The most dangerous health care professional is Highly experienced, confident but uneducated.

THANK YOU

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