Patient Assessment: Respiratory
System
NUR 409
Fall 2014-2015
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OUT LINE


a.
b.
c.
Regulation of respiration..
Assessment:
HX.
PE.
Diagnostic studies.
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Regulation of Respiration
*Respiratory Center
a. Pons= controls rate & depth of inspiration.
b. Medulla Oblongata= control rhythm of respiration.
** Chemoreceptor
a. Center-medulla oblongata:

Monitor arterial blood indirectly by sensing
changes in the PH of CSF.

Sensitive to very small changes in PH.

Increased levels of CO2= low PH== stimulates
respiratory center to increase depth & rate of
ventilation.
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b. Peripheral: aortic bodies & carotid bodies)
 Located
in aortic bodies of aortic arch &
carotid bodies at bifurcation of the
carotids.
 Primarily sensitive to changes in O2 levels
in the arterial blood, do detect changes in
CO2 & PH.
 As PaO2 & PH decrease= peripheral
chemo-receptors stimulate respiratory
center to increase ventilation.
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 Peripheral
chemoreceptors not sensitive
as central chemoreceptors
 PaO2 must drop to approximately 60
mmHg before the peripheral
chemoreceptors have much influence on
ventilation.
 It become the major stimulus to
ventilation when center chemoreceptors
are reset by chronic hypoventilation.
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Assessment of Respiratory Functions
Health History:
a.
b.
c.
d.
e.
f.
g.
h.
i.
j.
Dyspnea, Orthopnea, PND.
Cough,Throat soreness.
Sputum Production.
Chest pain (pleuritic, intercostal, generalized chest
pain).
Habit HX (smoking).
Occupational exposure to allergens/
environmental pollutants.
Past personal/ family health HX.
Voice changes.
Fatigue & weight changes.
medication
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Sputum production
Yellow, green, or brown sputum typically
signifies bacterial infection.
 clear or white sputum may signify absence of
bacterial infection.
 The color comes from white blood cells in the
sputum.
 Rust-colored sputum (yellow sputum mixed
with blood) may signify tuberculosis.

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Sputum production
Mucoid, viscid, or blood-streaked sputum
is often a sign of a viral infection.
 Persistent slightly blood-streaked sputum
is present in patients with carcinoma.
 Large amounts of clotted blood are
present in the sputum of patients who
have suffered a pulmonary infarct.

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Cough
cough can be stimulated by external agents, by
inflammation of the respiratory mucosa, or by
pressure on an airway caused by a tumor.
 caused by smoking, allergies, heartburn, asthma,
and certain medicationsfrom the patient about
the cough should include onset,
 precipitating factors, timing, frequency, and
whether the
 cough is productive or non.

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Past Medical History
Any lung problems such as asthma or
TB?
 Exposure to lung disease?
 Any chest surgery or diagnostic
studies?
 How many pillows do you use to sleep?
 Allergies?
 History of smoking?
 Medications? Vaccine?
 Any O2 use at home?

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Risk factors

Smoking
◦ Pack years = #of pack/day x # of years
Personal / family history
 Occupation
 Allergens
 Recreational exposure

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Assessment
◦ LOOK - LISTEN - FEEL







Look for Symmetry of Chest Expansion
Look for Signs of Increased Respiratory Effort
Look for Changes in Skin Color
Listen for Air Movement at Mouth & Nose
Listen for Air Movement in Peripheral Lung Fields
Feel for Air Movement at Mouth & Nose
Feel for Symmetry of Chest Expansion
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Physical assessment
Ch. Ch of respirations: Respiratory rate,
depth, and pattern of respiration
 Labored breathing, use of accessory
muscles
 Cyanosis of skin
 A/P diameter of chest, and patient
posture
 Chest expansion

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Physical assessment
Retractions: subclavicular, Substernal,
intercostals.
 Breathing Sounds.
 Sputum.
 Mental status.
 V/S.
 Chest deformities or scars
 IE ratio
 Position of trachea.

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Assess
Signs of Respiratory Distress





Nasal Flaring
Tracheal Tugging
Retractions
Accessory Muscle Use
Use of Abdominal Muscles on Exhalation
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Inspection of Chest:
Kyphosis, scoliosis, barrel chest.
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Inspect
Clubbing of the fingers
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Palpation
Tactile fremitus
 Subcutaneous emphysema
 Thoracic expansion
 Trachea

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Palpation
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Palpation
Symmetric expansion- place
hands of postero-lateral
chest wall with thumbs at
level of T9 or T10; Slide
hands medially to pinch up a
small fold of skin between
thumb; have person take a
deep breath your thumbs
should move apart
symmetrically
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Percussion
Flat percussion note is a soft, high-pitched
sound. It is more likely to be heard if a large
pleural effusion is present in the lung beneath
the examining hand.
 Dull percussion note is medium in intensity and
pitch. It is heard if atelectasis or consolidation
due to pneumonia, pulmonary edema, or
pulmonary hemorrhage.
 A tympanic drumlike sound is a high-pitched
noise heard if asthma or a large pneumothorax
is present.
 See Table (24-1).

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Percussion
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Percussion
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Auscultation

Tracheal breath sounds
◦ Over trachea, loud and harsh
 Bronchial breath sounds :Air in large
passageways,
◦ Over large airways they are normal; anywhere
else they are not normal

Bronchovesicular breath sounds
◦ Medium in pitch; heard over bronchioles
 Vesicular breath sounds: air filling the
alveolar sacs
◦ Heard over distal airway; quiet, low pitched
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Respiratory Sounds
Auscultation:
◦ Throat
◦ Intercostal spaces
◦ Triangle of auscultation
◦ Under the clavicle
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Auscultation
a. Evaluate the presence and quality of normal
breath sounds.
b. With flat diaphragm of stethoscope listen at
least one full respiration in each location
c. Compare side to side and top to bottom (
Go from left to right and then down or from
right to left and then down
d. analyze breath sounds
e. detect any abnormal sounds
f. examine sounds produced by spoken word
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Ausculatation
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Voice sounds
◦ Assessed when abnormalities noted
◦ Increased when sound travels through solid
or liquid
 Consolidation of lung, pneumonia, atelectasis,
pleural effusion, tumor, abscess
◦ Bronchophony: 99 – loud and clear
◦ Whispered Pectriloquy: 1, 2, 3 – loud
◦ Egophony – ‘E’ – heard as an ‘A’
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Adventitious Sounds

Snoring respiration
◦ Upper Airway
◦ Partial obstruction of the upper airway by the
tongue

Stridor
◦ High pitched crowing sound
◦ Usually heard on inspiration
◦ Indication of a tight upper airway
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Adventitious Sounds

Wheezing
◦ Whistling sound
◦ Usually heard on expiration
◦ Indication of narrowing of lower airways
caused by:
 Bronchospasm
 Edema
 Foreign material
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Adventitious Sounds

Rhonchi
◦ Rattling sound
◦ Caused by mucus in larger airways

Rales
◦ Fine crackling sound
◦ Indication of fluid in the alveoli
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Crackles
Indicate
 Atelectasis
 Bronchitis
 Pneumonia
 Pulmonary edema
 Pulmonary fibrosis (dry crackles
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Pulse Oximetry
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PaO2 and O2 saturation


PaO2 is the partial pressure of O2-measures
O2 dissolved in the plasma 3% of arterial
oxygen content.
O2 Saturation measures the amount of Hgb
saturated with oxygen. 97% of arterial content
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Pulse Oximetry



a.
b.
c.
d.
Measure O2 sat which reflects the arterial
oxygen saturation of hemoglobin (SaO2).
N value (93%-99%).
Reading is unreliable if pt:
On vasoconstrictor meds.
Has severe anemia.
Use IV dyes.
Smokers who have high levels of
carboxyhemoglobin.
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Pulse Oximetry
Percentage of O2 saturation =Amount of
O2 Hgb is carrying /amount of O2 Hgb
can cary
 (amount of O2 Hgb can cary =1.34)

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Oxyhemoglobin Dissociation Curve





Shows relationship between PaO2 and O2
saturation
These two values trend in the same direction
Curve allows us to estimate PaO2 based on noninvasive peripheral O2 saturation.
If the curve is shifted to the Rt it means decrease
affinity & increase perfusion.
If the curve is shifted to the Lt it means increase
affinity & decrease perfusion.
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PaO2 and O2 saturation
•it means increase affinity
& decrease perfusion.
Right shift
Acidosis
Hyperthermia
•it means decrease
affinity & increase
perfusion.
Hypercarbia
Left shift
Alkalosis
Hypothermia
Hypocarbia
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Factors That Affect the Oxyhemoglobin
Dissociation Curve
Right shift
Left shift
 Acidosis

 Hyperthermia

 Hypercarbia

Alkalosis
Hypothermia
Hypocarbia
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Oxyhemoglobin Dissociation
Curve

Clinical implications
◦ Right shift more common in high
acuity patients
◦ Body temperature can be controlled
to reduce oxygen consumption
Table 33-7
Conditions That
Alter Oxygen
Consumption
End-Tidal Carbon Dioxide Monitoring (ETCO2)
 Measures
the levels of CO2 at the end of
expiration when the percentage of CO2
dissolved in the arterioles (PaCO2) becomes
almost equivalent to percentage of alveolar
CO2 (PaCO2).
Therefore, ETCO2 can be used to
estimate levels of alveolar CO2.
Used to estimate PaCO2.
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ETCO2

ETCO2 values are obtained by
monitoring samples of expired gas from
an endotracheal tube, an oral airway, or a
nasopharyngeal airway.
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Mixed venous oxygen saturation (SvO2)





a parameter that can be measured to evaluate the
balance between oxygen supply and oxygen
demand.
For complete mixing of the blood, it is necessary
to obtain a blood sample from a pulmonary artery
catheter.
Normal mixed venous oxygen saturation is 60% to
80%
An SvO2 of 40% to 60% may occur in heart failure,
and values less than 40% may indicate profound
shock.
A decrease in SvO2 often occurs before other
hemodynamic changes
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Mixed venous oxygen saturation (SvO2)
A low SvO2 may be caused by a decrease in
oxygen supply to the tissues or an increase in
oxygen use due to a high demand.
 A decrease in oxygen supply results from low
hemoglobin, hemorrhage, or low cardiac output.
 increase in oxygen demand results from
hyperthermia, pain, stress, shivering, or seizures.
 Elevated SvO2 values are associated with
increased delivery of oxygen (high fraction of
inspired oxygen [FIO2]) or with decreased
demand from hypothermia, hypothyroidism, or
anesthesia.

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Diagnostic Test
a. Chest X-ray (CXR):




Used to detect anatomical structure of the
chest & diaghram.
Dense materials like the bones or heart
appear opaque or white.
Air filled space (lungs) appears black.
Soft tissue or fluid filled areas appear gray.
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Chest X-Ray
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Components of Pulmonary
Gas Exchange
Ventilation
 Diffusion

◦ Affected by pressure gradient,
surface area and thickness of
alveolar-capillary membrane

Perfusion
◦ Affected by hemoglobin (Hb)
concentration, affinity of oxygen to
Hb, and blood flow
Factors That Impair
Pulmonary Gas Exchange

Ventilation-perfusion
mismatching
◦ Pulmonary embolus
◦ Pneumothorax
Ventilation Perfusion Mismatch
Physiological Shunt (low V-P ratio)
pneumonia, atelectatsis, tumor
 Alveolar dead space (high V-P ratio)
Pulmonary infarction, Pulmonary embolism,
decrease COP
 Silent unit : when ventilation and
perfusion low,
ARDS, Pneumothorax

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b. Ventilation-Perfusion Lung Scan:
Detects the percentage of the lung that is normally
functioning.
 Diagnose & locate pulmonary emboli.
 Assess pulmonary blood supply.
 Is a nuclear imaging test composed of 2 parts:
a. Ventilation Scan: Inhalation of radioactive gas.
b. Perfusion Scan: radioactive materials given IV & scan to
visualize blood supply to lungs.
 Not useful diagnostic tool in pts who are dependent on
MV.

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Pulmonary Angiography:
 Rapid injection of radiopaque material into arm, femoral
vein, or pulmonary artery.
 Indicated for pulmonary embolism.
 The test indicates impaired blood flow to a vessel.
Sputum for cytology or analysis:
 indicated to examine for culture sensitivity.
Assess for cytology.
 Culture of acid-fast bacilli to detect the presence of TB &
mycobacterium.
 ( 3 serial specimens over 3 days).

 Before
taking the specimen to the lab, make
sure that you collected a sputum and not
saliva.
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Bronchoscopy





a.
b.
c.
Direct visualization of the larynx, trachea & bronchi by a flexible
fiber optic bronchoscope.
Indicated to detect tissues, collect secretions & obtain biopsy.
Examine the extent of the pathological problem.
Used to remove foreign bodies or lesions.
Patient Preparations:
CXR, ABG, Clotting studies.
IV sedation/ analgesia.
If purpose of Bronchoscopy is therapeutic (Drug that suppress
cough or secretions are avoided. (Intratopical anesthesia, atropine,
codeine).
Complications: laryngospasm, fever, dysrhythmias,
Pneumothorax, arrest, hemodynamic changes.
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Thoracentesis



a.
b.
c.
d.

a.
b.
c.
d.
Inserting a needle into pleural space.
Indicated to remove fluid/ or air, obtain specimen, give medication.
Patient Preparations:
CXR, Clotting studies.
Patient teaching.
Local anesthesia.
Pt in sitting position (chair, or edge of bed) e arms & shoulders up).
Post procedures:
Comfort measures.
Send specimen to lab.
Sterile dressing.
Assess for complications: Pneumothorax, respiratory distress, pain,
hypotension & pulmonary edema.
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Pulmonary/ or Ventilatory Function Test
Measures the ability of the chest &lungs to moves air
into & out of the alveoli.
 Pulmonary function tests help distinguish between
obstructive and restrictive pulmonary diseases.
 It include measurements of lung volume, capacity &
dynamic.
 The above measures are affected by age, disease,
exercise, gender, ht & body size.
a.Volume measurements (VT, IRV, EVR, RV).
b. Capacity measurements (IC, FRC,VC, TLC).
c. Dynamic measurements (provide information about
airway resistance & amount of energy expended in
breathing (work of breathing).

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Dynamic measurements








RR.
Minute Volume/ Ventilation: volume of air inhaled & exhaled /min.
Dead Space:
is the part of tidal volume that does not participate in alveolar gas
exchange.
Is the air contained in the airways (anatomical dead space 140 ml)
plus the volume of alveolar air that is not involved in gas exchange
(physiological dead space).
Calculated by subtracting the partial pressure of arterial carbon
dioxide (PaCO2) from the partial pressure of alveolar carbon
dioxide (PACO2).
N value of dead space in healthy adults is typically less than 40% of
the tidal volume.
The dead space-tidal volume ratio is used to follow the effectiveness
of MV.
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Residual volume: approximately 20% of
total lung capacity in young adult. Increase
e age.
 FEC: decrease in Ascitis and supine
position. Wt of abdomen contents forces
the diaphragm upward.
 Increase in recoil lung in pt e sarcoidosis.

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Lung Capacities
Composed of 2 or more lung volumes.
Useful measurements in clinical situation.
Total lung capacity: maximum lung volume after
full inspiration.
 At TLC, the force generated by a maximum
contraction of the inspiratory muscles equals
the recoil of the lung. That’s means: TLC
dependent on the strength of resp muscle &
elastic resistance of lung, chest wall,…..
 Its divided to 4 types.



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Lungs Volumes and Capacity
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CALCULATION
TLC= RV+IRV+TV+ERV.
 VC=IRV+TV+ERV=TLC-RV.
 FRC=RV+ERV.
 IC=TV+IRV.

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Dynamic Measurements
Alveolar Ventilation: The volume of tidal
air that is involved in alveolar gas exchange.
 This volume is represented as volume per
minute by the symbol VA.VA is a measure of
ventilatory effectiveness.
 It is more relevant to the blood gas values than
either the dead space or tidal volume because
these last two measures include physiological
dead space.
 VA is calculated by subtracting the dead space
(VD) from the tidal volume (VT) and multiplying
the result by the respiratory rate (f ):V.A =(VT .
VD )× f
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IMPORTANCE
 IN
RESTRICTIVE DISEASE:
 Decrease VC, decrease TLC, RV, FRC.
OBSTRCUTIVE
DIESEASE:
 Decrease VC, INCREASE TLC, RV, FRC.
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Arterial Blood Gases
Drawn from radial, femoral, brachial
arteries
 Invasive procedure
 Caution must be taken with patient on
anticoagulants
 Helps differentiate oxygen deficiencies
from primary ventilatory deficiencies
from primary metabolic acid-base
abnormalities

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Uses of Arterial Blood Gases

Indication of oxygenation status

Determination of acid-base state

Assess ventilation
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Acid Base Relationship

This relationship is critical for homeostasis

Significant deviations from normal ph ranges are
poorly tolerated and may be life threatening

Achieved by respiratory and renal systems
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ABG Normal Values






PaO2: 80-100 mmHg (partial pressure of oxygen
in arterial blood).
SaO2: 96-100% arterial O2 saturation.
pH: 7:35-7:45 over all state.
PaCO2: 35-45 mmHg respiratory component.
HCO3: 22-26 mEq/L (metabolic component).
BE: Base excess +2- -2
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Acid/base Relationship

H2O + CO2

H2CO3

Respiratory
HCO3 + H+
Metabolic
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Ratio of CO2 and HCO3
Normal ratio is 1 (CO2) to 20 (HCO3)
 Abnormal creates imbalance

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Respiratory Imbalances

Respiratory Acidosis
**********too much CO2

Respiratory Alkalosis
**********too little CO2
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Metabolic Imbalances

Metabolic Acidosis
*********too little HCO3

Metabolic Alkalosis
*********too much HCO3
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Know This
CO2 is an acid
 Regulated by the lungs
 Too much causes
acidosis




HCO3 is a base
Regulated by the
kidneys
Too much causes
alkalosis
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PH
 Indirect
measure of H+ ion concentration.
 Ratio of base (HCO3) to acid CO2.
 Acid give up (donate) H+ ions, while bases pick
up H+ ions.
 Body maintains a slightly alkaline pH of 7:357:45.
 Metabolic & Respiratory processes work
together to keep Hydrogen level (H+) in a
normal range.
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Regulators of Acid /Base
a. Buffers
 primary regulator.
 Act immediately.
 Present in blood & tissue.
 Take up extra H+ ions or release H+ (eg
bicarbonate, proteins & hemoglobin). a
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Buffer systems
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Regulators of Acid /Base
b. Respiratory system:
 Eliminates CO2.
 Respiratory center in medulla controls
breathing.
 Increased respirations leads to increased CO2
elimination from body & decrease CO2 in
blood.
 Decreased respirations leads to decrease CO2
elimination from body & increase CO2 in
blood.
 Responds within minutes to hours to changes in
Acid / Base.
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Regulators of Acid /Base
C. Renal System
Secrets H+ ions & reabsorbs bicarbonate
(HCO3) ions.
 Reabsorbing & secretion of electrolytes
like (Na, K).
 Responds within hours to days.
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What Are the Compensations?
In chronic respiratory acidosis
(COPD) the kidneys increase
The elimination of H+ and
absorb more HCO3. The ABG
will show NL ph, CO2 and
HCO3
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ABG Normal Values
PaO2:
80-100 mmHg (partial pressure of
oxygen in arterial blood).
SaO2: 96-100% arterial O2 saturation.
pH: 7:35-7:45 over all state.
PaCO2: 35-45 mmHg respiratory
component.
HCO3: 22-26 mEq/L (metabolic
component).
BE: Base excess +2- -2
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ABGs
 Acidemia: Acid
PH < 7.35.
condition of the blood in which
 Alkalemia: Alkaline
which PH >7.45.
condition of the blood in
 Acidosis: the
process causing acidemia.
 Alkalosis: the
process causing alkalemia.
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How to obtain ABGs
Hepranized syringe.
Blood from artery.
On Ice.
Prompt delivery to lab.
Include:
a. Time drawn.
b. FIO2.
c. O2 delivery rate & method (ventilatory
method).
d. Patient temperature.
e. Pulse Oximetry O2 saturation.




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Interpretation of ABGs
a. Evaluate PH: this determines acidosis or
alkalosis.



7.40 is the middle of the normal range of 7.35-7.45.
Value below 7.40 is moving toward acidosis.
Value above 7.40 is moving toward alkalosis.
b. Evaluate Respiratory component
(PaCO2):


If PaCO2 < 35, the value is alkalotic.
If PaCO2 > 45, the value is acidotic.
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Interpretation of ABGs
c. Evaluate metabolic component (HCO3):


If HCO3 > 26 mEq/L, the value is alkalotic.
If HCO3 <22 mEq/L, the value is acidotic.
d. Determine which component (PaCO2 or HCO3) matches the PH.
e. If
the PH is increased or decreased is the underlying
disorder respiratory or metabolic:
Respiratory:
Decrease PH, Increase PaCO2.
Increase PH, Decrease PaCO2.
Metabolic:
Decrease PH, Decrease HCO3.
Increase PH, Increase HCO3.
If both respiratory & metabolic components match the
PH, may be it is a mixed disorder.
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Interpretation of ABGs
e. Determine the degree of compensation:
a.
Absent:
* The PH is not within normal range.
** The components (CO2 & HCO3) that does not match the PH
imbalance is still within its normal range.
b.
Partial:
* The PH is not within normal range.
** The components (CO2 & HCO3) that does not match the PH
disorder is below or above the normal range.
C.
Complete:

The PH is within normal range, & both CO2 & HCO3 are
either above or below normal range.
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Metabolic Acidosis
Ph
7.30
Paco2 40
Hco3
15
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Metabolic Acidosis
 Failure



of kidney function.
 Blood HCO3 which results in  availability of
renal tubular HCO3 for H+ excretion
Ph < 7.35
Hco3 < 22
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Causes of Metabolic Acidosis
 Renal
failure

Diabetic ketoacidosis

Lactic acidosis

Excessive diarrhea
 Cardiac
arrest
 Poisoning
(acetylsalicylic acid)
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S&S
 Lethargy
 Nausea
& Vomiting.
 Dysrhythmia.
 Coma.
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Treatment of Metabolic Acidosis
RX of underlying cause.
 Monitor I&O.
 Monitor for dysrhythmia.
 Protect against infection.
 Give sodium bicarbonate.

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Respiratory Alkalosis
 Ph
7.50
 Paco2
30
 Hco3
22
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Causes of Respiratory Alkalosis
 Hyperventilation
 PE.
 Panic disorder
 Brain stem disease.
 Pain
 Anxiety
 Pregnancy
 Acute anemia
 Salicylate overdose
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S&S
Dizziness.
 Tingling.
 Numbness.
 Restlessness.
 Agitation.
 Tetany.

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Treatment of Respiratory Alkalosis
Sedation.
 Reassure &Support patient.
 Breath in paper bag for attack of
hyperventilation.
 Decrease RR.
 Decrease tidal volume.

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Metabolic Alkalosis
 pH
7.50
 PCO2
 HCO3
40
30
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Metabolic Alkalosis



plasma bicarbonate
pH > 7.45
HCO3 > 26
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Causes of Metabolic Alkalosis
  loss acid
 Diuretics.
from stomach or kidney
 Adrenal disease.
 Corticosteroid therapy


excessive alkali intake (Sodium bicar over load).
hypokalemia
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S&S
Dullness.
 Weakness.
 Dysrhythmias.
 Tetany.
 Hypokalemia.

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Treatment of Metabolic Alkalosis
Treatment of underlying cause.
 Monitor I & O.
 K replacement therapy.
 Ammonium chloride.

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Respiratory Alkalosis
 Too
much CO2 exhaled (hyperventilation)

 PCO2, H2CO3 insufficiency =  ph


Ph > 7.45
Pco2 < 35
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Respiratory Acidosis
 Ph
7.30
 Paco2
60
 Hco3
26
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Respiratory Acidosis
 Too
 pH
much CO2
< 7.35
 CO2
> 45
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Causes of Respiratory Acidosis
Neuromuscular
disease
Head
injury
Sedatives, narcotics
Atelectasis
Obstructed airway (COPD).
Inappropriate vent settings
Alveolar hypoventilation
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S&S
Dyspnea.
 Headache.
 Mental confusion.
 Pallor.
 Sweating.
 Apprehension, restlessness.

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Treatment of Respiratory Acidosis
Aggressive CHEST PHYSIOTHERAPY.
 SUCTION.
 INCREASE RR.
 INCREASE TIDAL VOLUME.

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ABG Analysis(example)
pH 7.21, Pa02 70mmHg, PaCO2 63mmHg,
HC03 27mEq/L
1. Evaluate the pH. pH is not in normal
range, but is decreased (acidosis).
2. Evaluate the PaC02. PaC02 is elevated.
3. Evaluated the HC03. HC03 is slightly
elevated
4. Describe the acid base status.
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Step 1
 Evaluate
the pH
 Normal 7.35-7.45
 Below 7.35=acidemia
 Above 7.45= alkalosis
 If a pt has more than one acid-base
balance at work, the pH identifies the
process in control
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Step 2
 Evaluate
ventilation
 Normal 35-45mmHg
 greater than 45= ventilatory failure and
respiratory acidosis
 less than 35 = alveolar hyperventilation
and respiratory alkalosis
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Step 3
 Evaluate
metabolic process
 Normal 21-25
 HCO3 < 22 = metabolic acidosis
 HCO3 > 25 = metabolic alkalosis
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Step 4
 Determine
primary and compensating
disorder
 When both PCO2 and HCO3 are
abnormal, one reflects the primary acidbase disorder and the other reflects the
compensating disorder
 To decide which is which, check the ph
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Step 4
3 states of compensation possible
 1. Non compensation- alteration of only

pco2 or HCO3
 2. Partial compensation- when both pco2 and
HCO3 are abnormal and because compensation
is incomplete, the ph is also abnormal;
 3. Complete compensation- when both pco2
are abnormal, but because compensation is
complete, the ph is normal
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Step 5
 Evaluate
oxygenation
 Normal 80-100mmhg
 PO2 60-80 = mild hypoxemia
 PO2 40-60= moderate hypoxemia
 PO2 below 40 = severe hypoxemia
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Step 6
Interpret
Final
analysis should include
Degree of compensation
The primary disorder
The oxygenation status
Ex-”partially compensated respiratory
acidosis with moderate hypoxemia
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What Are the Compensations?
 Respiratory
acidosis

metabolic alkalosis
 Respiratory
alkalosis 
metabolic acidosis
 In
respiratory conditions, therefore, the kidneys
will Attempt to compensate and visa versa
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BE: refer to an excess or deficit,
respectively, in the amount
of base present in the blood.
 indicates whether the patient is acidotic
or alkalotic. A negative base excess
indicates that the patient is acidotic. A
high positive base excess indicates that
the patients is alkalotic.

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Base excess beyond the reference range
indicates
 metabolic alkalosis if too high (more than
+2 mEq/L)
 metabolic acidosis if too low (less than −2
mEq/L)

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Anion Gap
 Its
normal to have approximately the same n of
anions and cations circulating in blood . Some of
them not measured anion gaps is present.
 Helps determine presence and cause of
metabolic acidosis
 (Na + K)-(Cl + HCO3) = anion gap
 Normal value is 6-15 (3-11)
 15 or less is loss of base
 16 or more gain of acid (increase in n of
unmeasured anion , lactate, ketone bodies…).
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The serum anion gap is useful for determining
whether a base deficit is caused by addition of
acid or loss of bicarbonate.
 Base deficit with elevated anion gap indicates
addition of acid (e.g., ketoacidosis).
 Base deficit with normal anion gap indicates
loss of bicarbonate (e.g., diarrhea). The anion
gap is maintained because bicarbonate is
exchanged for chloride during excretion.

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Final Analysis
 Compare
to previous ABG
 Look at patient’s history and present
situation
 Determine what is needed to correct
situation
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Case Study #1
Mr. Adams is a 60 y/O with pneumonia. He
is admitted with dyspnea, fever, and ABG
pH 7.28
CO2 56
PO2 70
HC)3 25
SaO2 89%
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Answer

Uncompensated respir acidosis with
hypoxemia due to pneumonia. Inadequate
ventilation and perfusion. Goals improve
both vent an oxygenations. Minimum o2
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Case #2
Ms. Stan is a 24 year old college student.
She has a history of Crohn’s disease c/o 4
day history of boody diarrhea. An ABG is
obtained:
 pH 7.28
 CO2 43
 PO2 88
 HCO3 20
 SaO2 96%

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Answer

Uncompensated metabolic acidosis.
Excessive loss from diarrhea. No
compensation, treat control diarrhea
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Case # 3
Mr. Like is a 89 y/O nursing home
resident admitted with urosepsis. Over
the last 4 hours he has developed SOB
and is confused. ABG:
 pH 7.02
 CO2 55
 pO2 77
 JCO3 14
 O2Sat 89%

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Answer

Meta is secondary to resp failure.
metbolic and resp acidosis with
hypoxemial Metabolic is caused by sepsis
, The respopressor, acidosis is secondary
to resp faiure. ARDS. Treatment is
aggressive, mech vent.Vasopressors,
bicarb
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Case # 4
Mrs Lander is a thin, 61y/o COPD patient.
Her ABG:
 pH 7.37
 CO2 63
 pO2 58
 HC)3 35
 SaO2 89%

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Answer

Lander has a fully compensated resp
adidosis with hypoxmia. Full
compensation normal pH in spite of
adid/base disorder. No treatment
baseline
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Case #5
Mrs. Doubtfire is found pulseless and not
breathing. After a couple minutes she
responds with a pulse and is breathing.
ABG:
 pH 6.89
 CO2 70
 pO2 42
 HCO3 13
 SaO2 50%

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Answer

Severe metabolic an resp acidosis with
hypoxemia. Resp component comes from
decreased perfusion, resp comp comes
from inadeq ventilation. Treatment is
intubation, mech vent
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Case #6
You find Mr. Aster in respiratory distress.
H/O diabetes and is febrile. ABG:
 pH 7.00
 CO2 59
 pO2 86
 HCO3 14
 Sao2 91%

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Answer
Metabolic and respiratory acidosis
hypoxemia. Resp acidosis from
pneumonia. Pneumonia has altered his
glucose metabolism hyperglycemia and
diabetic ketoacidosisl
1. Increase oxygenation, treat pneumonia,
administer IV fluids to treat DKA

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Quiz
A 42-year-old male patient had burns over
60% of his body surface area. On
admission, his BP was 95/60 mm Hg with a
heart rate of 132, respiratory rate of 8,
temperature 96[degrees] F (35.5[degrees]
C), and SaO2 of 90%. He was oliguric. He
was receiving I.V. infusions of propofol and
morphine.You use the five-step approach
to analyze his ABGs:
 * PaO2 of 63 mm Hg and SaO2 of 90%
suggest hypoxia based on his age

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Quiz
* pH of 7.20 is consistent with acidosis
 * PaCO2 of 52 mm Hg indicates
inadequate pulmonary ventilation to blow
off CO2
 * HCO3- of 17 mEq/L suggests a
metabolic alteration toward acidosis

Mixed respiratory and metabolic acidosis
with hypoxia
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Follow this five-step approach to interpreting your
patient's ABGs.
1. Is the patient hypoxic? Look at the Pao2 and Sao2.
2. What is acid-base balance? Check the pH.
3. How is pulmonary ventilation? Look at the Paco2.
4. What is the metabolic status? Review the HCO3-.
5. Is there any compensation or other abnormalities?
What is the primary cause of acid-base imbalance
and which derangement is the result of secondary
(compensatory) change?
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