Nur 260 Exam : Alterations In Oxygenation Notes
ALTERATIONS IN OXYGENATION
Alveoli - Functional unit of lung interconnected by pores of Kohn that produce surfactant;
▶ Each adult has 300 million alveoli arranged in clusters which are surrounded by capillary bed
▶ Gas exchange occurs via diffusion and depends on ventilation-perfusion ratio
▶ Normal –fully-functional alveoli & good blood supply allow for maximum gas exchange
▶ Impaired Gas exchange:
▶ Alveoli is constricted, blocked or collapsed; blood passes alveoli without max gas exch.
▶ Blood supply is blocked not giving alveoli adequate blood
supply Lung Tissue Properties:
▶ Compliance – Expandability of lung which depends on surface tissue of alveoli & connective tissue of lungs →
elastin gives lungs stretchability
▶ Normal – easily stretched when take a deep breath
▶ Low – stiff/difficult to inflate → pulmonary fibrosis or morbid obesity
▶ High – lungs lost elasticity (overdistended) → returning CO2 such as with emphysema r/t loss of some
alveolar wall→ lose recoil → overinflation
▶ Elastic Recoil – ability of lungs to reduce in volume after being
stretched Respiratory Defense Mechanisms –
▶ Filtration of air
▶ Mucocilliary Clearance
▶ Cough reflex
▶ Reflex Bronchoconstriction
▶ Alveolar Macrophages
Respiratory System Age Related Changes - respiratory peak @ age 25
▶ Lifetime exposure to environmental stimuli – pollution; occupational hazards
▶ Concurrent chronic disease – CAD, CHF, DM, COPD, alcoholism
▶ Structural alterations – decr ability to take a deep breath; diminished vital capacity ( max amt of air inhaled
& exhaled in a cycle)
◦ ↓ in elastic recoil
◦ ↓ in chest wall compliance
◦ AP diameter increases
◦ Kyphoscoliosis with advancing age
◦ Alveolar surface decreases
▶ Defense Mechanism Changes – decr ability to clear secretions, incr URI, Incr r/f aspiration
◦ ↓in cilia function
◦ ↓cough reflex
◦ ↓effectiveness of alveolar macrophages
◦ Muscle atrophy of pharynx and larynx
▶ Decrease in Physical Mobility – pulling of secretions in lungs → r/f
pneumonia Respiratory Assessment Interview
▶ Current respiratory problem
◦ Restlessness → 1st indication of problem with oxygenation
◦ changes in breathing pattern/dyspnea
1
, ▶ dyspnea – shortness of breath → @ rest, exercise, climbing stairs??; factors that
relieve/worsen; sudden/gradual; lying flat?; S/S of other diseases (CHF, anaphylaxis, etc.)
◦ cough/sputum – onset/time (if AM w/ sputum → bronchitis); COCA
◦ chest pain – inhale/exhale, coughing, musculoskeletal condition, cardiac or GI in origin
◦ Adventitious lung sounds
▶ History of Respiratory Disease
▶ Lifestyle
▶ Allergies
▶ Medication history
Physical Exam/Assessment
▶ Inspection
◦ Anatomy of nares – patency, deformity, mucous membranes; mouth – color, lesions, tongue
symmetry; pharynx – smooth & moist w no evidence of exudates or ulcerations
◦ Breathing pattern – distress? RR, depth, rhythm, inspiration half as long as expiration;
abnormal patterns?
◦ Chest configuration – AP diameter: barrel → COPD; hyposcoliosis; obesity effect on breathing
◦ Skin color – cyanosis in lips, palm, under tongue
◦ Clubbing of fingernails – chg in angle w/ finger nail fr base to tip; incr in depth & bulk @ fingertips
▶ Palpation
◦ Tracheal position - midline
◦ Thoracic expansion – symmetry → place hands @ 10 th rib look for equal movement; unequal →
pneumothorax, hemothorax, pleural effusion; decr chest expansion – COPD, neuromuscular
disease (ALS)
◦ Tactile fremitus – vibration of chest wall produced by vocalization: most prominent by sternum b/t
scapulae – place palm on chest or back & ask pt to say ‘99’; incr w/ pneumonia & decr w/
emphysema (air trapped)
▶ Percussion
◦ Resonant – low pitch over all lung fields
◦ Hyperresonant – overinflation of lungs → COPD
◦ Dull (thud/muffled) – pneumonia/pleural effusion
▶ Auscultation
◦ Normal (bronchial – either side of trachea; bronchovesicular-either side of sternum over main
bronchus, vesicular-alveoli)
◦ Adventitious (crackles, rhonchi, wheezes, pleural friction
rub) Diagnostic Tests
▶ CBC
▶ ABGs
▶ Pulse Oximetry
▶ Pulmonary Function Test – good dx aide for COPD and can be used sequentially to
determine dysfunction/response to treatment
▶ CXR, CT of lung
▶ Sputum studies
▶ Ventilation-perfusion – pleural effusion
▶ Peak expiratory flow rate (PEFR) – asthma treatment w/ asthma action plan (qAM or w/ S/S)
▶ Exercise test – 6 or 12 min for desaturation
▶ Bronchoscopy with possible lung biopsy – sputum sample/biopsy of masses (NPO fr midnite d/t
2
, conscious sedation; post – check VS, LOC & gag reflex; NPO until gag reflex returns
▶ Thoracentesis
Nursing Dx (can be R/F depending on data collected)
▶ Ineffective Breathing Pattern
▶ Ineffective Airway Clearance
▶ Impair Gas Exchange
▶ Activity Intolerance or Fatigue
▶ Ineffective Tissue Perfusion
▶ Imbalance Nutrition < Body
Requirements Nursing Interventions
▶ Positioning of the client → 1st thing to do 30-45* if shortness of breath/difficulty breathing
▶ Coughing and breathing exercises – promotes lung expansion; Huff/purse - COPD
▶ Nutritional support – breathing reqs energy
▶ Hydration (oral or intravenous) – 2-3L q 24hr
▶ Supplemental oxygen
▶ Oral and nasal suctioning – for ineffective cough
▶ Smoking cessation
▶ Current on vaccinations – flu & pneumococcal
▶ Medication administration
◦ Antibiotics - infection
◦ Bronchodilators - obstructive
◦ Mucolytics and Expectorants – promote cough & secretions
◦ Corticosteroids – anti-inflammatory
▶ Exercise - improves lung function
▶ Rest and Assistance with ADLs
UNDERSTANDING ABGs
▶ A diagnostic tool to analyze a patient’s oxygenation status and acid-base balance
▶ Will give you information if the body is attempting to compensate for the imbalance
▶ Acid-base imbalances are conditions and are not disease states → result of underlying
pathology Values – ROME – respiratory opposite / metabolic equal
Less than Normal Greater than
pH ACIDOSIS 7.35-7.45 ALKALOSIS
PaCO2 (Respiratory) ALKALOSIS 35-45 ACIDOSIS
HCO3 (Metabolic) ADICOSIS 22-26 ALKALOSIS
paO2 80-100
▶ pH labels it Acidosis or Alkalosis
▶ What matches determines if Respiratory or Metabolic
▶ Ex. pH 7.3 acid PaCO2 47 acid HCO2 24 normal; pH makes it acidosis which matches CO2 acidosis,
therefore respiratory acidosis
Respiratory System (PaCO2)
▶ Regulates acid-base by eliminating or retaining CO2
▶ Medulla oblongata is the brain’s respiratory center
▶ Responds to changes in pH within minutes, but it is less effective over time
▶ If respiratory system is cause of imbalance it cannot correct it; must be corrected by renal
system Renal System (HCO3 – bicarb)
▶ Kidneys conserve and reabsorb all the HCO3 it filters as well as excreting weak acids
▶ Respond to changes in pH slowly (2-3 days) but is it more powerful
3
, ▶ If kidneys are cause of acid-base imbalance it cannot correct the problem, but respiratory
will Respiratory Acidosis – pH<7.35, PaCO2>45 - Accumulation of CO2 which then decreases pH of
blood
▶ Caused by:
▶ CNS depression r/t medications or head/brain injury/trauma (incl. tumor, CVA)
▶ Hypoventilation – r/t pain, deformity, chest wall injury, abdominal distention
▶ Pulmonary disorders – atelectasis, pneumonia, pneumothorax, pulmonary edema, COPD
▶ Impaired respiratory function – r/t neuromuscular disorders & NM blocking drugs
▶ Foreign body aspiration
▶ Respiratory muscle weakness (Spinal cord injury, Guillain-Barre)
▶ Mechanical hypoventilation
▶ S/S → dyspnea, shallow respirations, HA, restlessness, tachycardia, dysrhythmias
Respiratory Alkalosis – pH>7.45; PaCO2<35 - Release of CO2 which then increases pH of
blood
▶ Caused by:
▶ Hyperventilation – anxiety, pn, incr metabolic demands (fever, pregnancy, sepsis), mechanical ventilator
▶ Initially a response to hypoxia (pneumonia, HF, PE, etc.) → can’t sustain increased RR so pt falls
into hypoventilation → acidosis
▶ S/S – lightheadedness, confusion, numbness & tingling, dysrhythmias, palpitations, diaphoresis & dry
mouth Metabolic Acidosis – pH<7.35; HCO3<22 - Deficit of base in bloodstream OR excess of acids other than CO2
▶ Caused by:
▶ Excess acids –
▶ Lactic Acidosis – accumulates in anaerobic metabolism
▶ Ketoacidosis related to diabetes, starvation or alcoholism
▶ Renal failure
▶ Starvation
▶ Shock
▶ Base deficit –
▶ Diarrhea
▶ GI fistulas
▶ S/S – HA, confusion, restlessness, dysrhythmias, warm flush skin, Kussmaul’s respirations (incr RR w/ fruity
odor) Metabolic Alkalosis – pH>7.45; HCO3>26 - Loss of acid OR excess of base in bloodstream
▶ Caused by:
▶ Loss of acid
▶ Vomiting or gastric suctioning
▶ Diuretic therapy
▶ Excess base
▶ Excess bicarb administration – antacids or lactate in dialysis
▶ Excess steroid
▶ S/S – respiratory depression, dizziness, loss of energy, weakness, muscle twitching & cramping,
Disorder
N/V Assessment of Oxygenation Compensation ABGs
▶ PaO2
Respiratory Acidosis
is the amount of oxygenKidneys conserve
dissolved bicarbNormal values
in plasma Decrease
80-100in pH
pH <▶7.35
PaO2 >70 is usually adequate toifbuffer
personexcess acid
is hemodynamically Increase in PaCO2
stable
CO2▶> 45SaO2 is the % of oxygen bound to hemoglobin, normal value > 95 Increase
→ if noinchronic
HCO3 ifillness
▶ Oxygen-Hemoglobin Dissociation Curve compensating (>26)
Compensation
▶ When
Respiratory there is an acid base imbalance,
Alkalosis the body
Kidneys excrete attempts of compensate.
bicarb Increase inThe
pH respiratory and renal
systems
pH > 7.45 compensate for each other to return
To minimize alkalosisthe pH to normal (the 20:1 ratio)
Decrease in PaCO2
CO2▶< 35The goal of compensation is a normal pH (7.35-7.45) Decrease in HCO3 if
▶ The system not causing the problem tries to correct the imbalance compensating (<22)
▶ The lungs compensate
Metabolic Acidosis Rateforand
metabolic
depth ofdisturbances by changing
DecreaseCO2 excretion
in pH
▶ pH < 7.35 respirations increase, Decrease in
The kidneys compensate for respiratory disturbances by altering bicarb. HCO3
HCO3 < 22 eliminating CO2 Decrease in PaCO2 if
4 compensating (<35)
Metabolic Alkalosis Rate and depth of Increase in pH
pH > 7.45 respirations decrease, Increase in
HCO3 > 26 Retain CO2 HCO3
Increase in PaCO2 (>45)
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