Resident Resp Failure Lecture about respiration center

MohitSharma179329 72 views 39 slides Sep 10, 2024
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About This Presentation

Acute respiratory failure in children is most common , mainly occurr in tha age of 5- 7 year of age


Slide Content

Definitions: Acute Respiratory
Failure
ARF is the inability of the respiratory system to
deliver O
2
and remove CO
2
at a sufficient rate to
meet the body’s metabolic demands
Can be hypoxic or hypercarbic
ABG abnormalities
–PaCO
2
> 55 mm Hg (with low pH)
–PaO
2
< 60 mm Hg
–SaO
2
< 90% (in absence of cyanotic CHD)

Problems with Oxygenation
Hypoxemia: Decrease in tissue O
2 delivery
–Hypoxic Hypoxemia -- Lung Disease
–Ischemic Hypoxemia -- Decreased Blood Flow
-- DO
2
= O
2
content x Cardiac Output
–Anemic Hypoxemia -- Decreased O
2
-Carrying
Capacity
-- O2 Content = (1.39 x HgB x SaO
2
) + (0.003)
(PaO
2
)

Hypoxic Hypoxemia: Where is the
problem?
FIO
2
(Ex. Altitude)
Decreased Air Entry
-- Sedation (Ex. Opioid Overdose)
-- Respiratory Muscle Weakness (Ex. SMA)
-- Airway Obstruction (Ex. Croup, Asthma, etc)
V/Q Mismatches (Ex. Atelectasis, ARDS)
Shunting (Ex. CHD, pulmonary hypertension)
Diffusion Abnormalities (Ex. Pulmonary Fibrosis,
ARDS)

Acute Respiratory Failure:
Problems with Ventilation
Hypercapnea (increased CO
2) can be seen with:
1. Increased Dead Space (areas not involved in
gas exchange) (Ex. Asthma, Pulmonary HTN)
2. Decreased Alveolar Ventilation
- Decreased Tidal Volume or Respiratory Rate
(Ex. Coma, Overdose, MG, ARDS, etc)
3. Obstructed Airways (Ex. Asthma)
4. Increased CO
2
production (Ex.
Burns,Overfeeding)
CO
2
diffuses easily across alveolar-capillary membrane so
diffusion problems usually do not cause hypercapnea

Acute Respiratory Failure: How to
Diagnose
Clinical Exam -- MOST IMPORTANT
1. Changes in RR and Breathing Effort:
Question - Why do infants “tire out?”
2. Changes in lung exam (stridor, wheeze, etc.)
3. Cyanosis – definition?
Flushing, tachycardia, HA, confusion – seen with
acute hypercarbia
Mental Status

Chronic
Hypoxemia/Hypercarbia
Clinical signs/lab evidence of chronic
hypoxia:
-- Clubbing – seen with chronic hypoxemia
-- What might you see on abdominal
exam?
-- Labs: Polycythemia
Lab evidence of hypercarbia

Hypoxic Hypoxemia: How to
Diagnose
Pulse oximetry – How does it work? What
are its limitations?
Arterial Blood Gas – What information does
this provide that pulse-ox does not?

Pulse-oximetry: How does it work?
Current pulse-ox machines measure 2 types
of light: red (wavelength=660 nm) and
infrared (wavelength= 940 nm)
Red light is better absorbed by deoxy-Hgb,
infrared light is better absorbed by oxy-
Hgb, so the ratio gives you the SaO
2

Pulse-oximetry Problems
1. Doesn’t work well with poor perfusion
2. Other light sources (Ex. phototherapy
light) can interfere with the results
3. Abnormal Hgb can lead to overestimation
of a true SaO
2 (specifically carboxy-, and
metHgb)
What laboratory test do you order in
someone with met- or carboxy-hgb

Arterial Blood Gas and
Oxygenation
ABG – can give you carboxy and metHgb
levels (if you ask); will give you co-
oximetry values (multiple wavelengths
measured)
-- will also give you a PaO
2 which can
help you diagnose a patient with
hypoxemic hypoxia using an equation
called ………..

Alveolar Gas Equation
PAO
2 = FIO
2(P
B-P
H2O) – PCO
2/R
–PAO
2 = Alveolar oxygen partial pressure
–FIO
2
= fraction of inspired oxygen
–P
B
= barometric pressure (760 mm Hg at sea
level)
–P
H2O = partial pressure of water vapor (47 mm
Hg)
–PCO
2
= partial pressure of CO
2
–R = respiratory quotient (usually ~ 0.8)

Alveolar Gas Equation
So at room air at sea level, your PAO
2
should be 100
On 100% FIO
2 at sea level, your PAO
2
should be 663
The difference between Alveolar (PAO
2
) and
arterial (PaO
2) oxygen is called the A-a
gradient and should be less than 20; this
will help you figure out if this is hypoxic
hypoxemia and the degree of hypoxia

Given a PaO
2
, what is the SaO
2
(and vice-versa)
Curve moves to right with
Lower pH
Higher Temperature
Increased 2,3 DPG

Hypercarbic Respiratory Failure:
Who cares about CO
2 and pH?
What makes you breathe?
Primarily pH (can be PaO2 in some patients)
What happens to you if you are too alkalotic or acidotic?
Acidosis: AMS, impaired cardiac contractility, pulmonary
vasoconstriction, metabolic abnormalities, etc.
Alkalosis: tetany (sec. to decreased iCa), arrhythmias, etc.
Does it matter what the source of the altered pH is?
Yes. For example: metabolic acidosis is worse for you than
respiratory acidosis.

Arterial Blood Gas, pH, and
Ventilation
pH < 7.35 with high CO
2: respiratory
acidosis
pH > 7.35 with high CO
2: compensated
respiratory acidosis
pH < 7.35 with low bicarb: metabolic
acidosis
pH > 7.35 with low bicarb: compensated
metabolic acidosis
What is a base deficit?

Base Deficit
Given a normal pCO2, how much base would
be needed to correct the pH.
Ex. 7.35/28/80/-15

Arterial Blood Gas, pH, and
Ventilation
pH > 7.45 with low CO
2: respiratory alkalosis
pH < 7.45 with low CO
2
: compensated
respiratory alkalosis
pH > 7.45 with high bicarb: metabolic
alkalosis
pH < 7.45 with high bicarb: compensated
metabolic alkalosis

How to Approach an ABG
First – Is this an arterial or venous blood gas?
Second - does the patient have an acidosis or an
alkalosis
–Look at the pH
Third, what is the primary problem – metabolic or
respiratory
–Look at the pCO
2
–If the pCO
2 change is in the opposite direction
of the pH change, the primary problem is
respiratory
–You never overcompensate

How to Approach an ABG
Next, don’t forget to look at the
effectiveness of oxygenation, (and look at
the patient)
–your patient may have a significantly
increased work of breathing in order to
maintain a “normal” blood gas
–metabolic acidosis with a concomitant
respiratory acidosis is concerning

Case 1
Sameer got into some of Dad’s barbiturates.
He suffers a significant depression of
mental status and respiration. You see
him in the ER 3 hours after ingestion with
a respiratory rate of 12. A blood gas is
obtained. It shows pH = 7.16, pCO
2 = 70,
HCO
3
= 22

Case 1
What is the acid/base abnormality?
1.Uncompensated metabolic acidosis
2.Compensated respiratory acidosis
3.Uncompensated respiratory acidosis
4.Compensated metabolic alkalosis

Case 2
You are evaluating a 15 year old female in the
ER who was brought in by EMS from school
because of abdominal pain and vomiting.
Review of system is negative except for a 10
lb. weight loss over the past 2 months and
polyuria for the past 2 weeks. She has no
other medical problems and denies any
sexual activity or drug use. On exam, she is
alert and oriented, afebrile, HR 115, RR 26
and regular, BP 114/75, pulse ox 95% on RA.

Case 2
Exam is unremarkable except for mild abdominal
tenderness on palpation in the midepigastric
region and capillary refill time of 3 seconds. The
nurse has already seen the patient and has sent
off “routine” blood work. She hands you the
result of the blood gas. pH = 7.21 pCO
2
=

24
pO
2
= 45 HCO
3
= 10 BE = -10 saturation =
72%

Case 2
What is the blood gas interpretation?
1. Uncompensated respiratory acidosis with
severe hypoxia
2. Uncompensated metabolic alkalosis
3. Combined metabolic acidosis and respiratory
acidosis with severe hypoxia
4. Metabolic acidosis with respiratory
compensation

Case 3
10 year old with history of ALL and
neutropenia presents with tachypnea. He
has no O
2
requirement but is breathing 30
– 40 times/minute. Lung exam (other than
the tachypnea) is normal. CXR shows no
infiltrate. An ABG is done: 7.45/30/90/22
on room air. Does this patient need a
bronchoscopy to diagnose his respiratory
compromise? Why or why not?

Case 3
Answer: No; This is a trick question
because he doesn’t have respiratory
compromise
The patient is tachypneic for some other
reason than acidosis, hypercarbia, or
hypoxia (i.e. increased intracranial
pressure, burgeoning sepsis, etc)

Other Laboratory Findings in ARF
CXR Abnormalities
Complete Blood Count (look at WBC and
Hgb, which may suggest chronic hypoxia)
Electrolyte Abnormalities (look at
bicarbonate)

Foreign Body Aspiration

Right Lung
Atelectasis

Left Lung
Pneumonia
with Effusion

Pneumothorax

ARDS
(Bilateral
Infiltrates)

Flail Chest

ARF -- Treatment
Surgical: Thoracostomy tubes
Medications:
– b-agonists
–Anticholinergics
– Anti-inflammatory agents (steroids, NSAIDS)
–Surfactant
–Nitric Oxide

ARF -- Treatment
Monitoring
–invasive (ABG, PAC) or noninvasive (pulse-
oximeter)
Prevention
–Encourage coughing, frequent position
changes, reflux precautions, decompress
abdomen, etc.

ARF -- Treatment
O
2 Delivery Systems: Low vs. High Flow
Low Flow:
–Nasal Cannula: FIO
2 < 40% (1L/min ~ 3%)
–Blow-by O2
High Flow:
–Head Hood: Flow >10 l/min
–Venturi Face Masks: FIO
2
~ 50%
–Nonrebreather Mask: FIO
2
~ 80-100%
–Bag-Mask-Valve Units: FIO
2 ~ 100%

ARF -- Treatment
Continuous or Bilevel Positive Pressure
(CPAP or BIPAP) -- applied through a
tight-fitting mask
Best applied in an awake, cooperative
patient who is expected to improve in 48-
72 hours.

ARF – Treatment with Mechanical
Ventilation
Name - saini
omprakash
Group - 70
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