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Objectives
SOURCES OF ACIDS
Waste products of CHO,(converted to free H
ions)
Protein, and fat metabolism
CO2 : waste product of glucose breakdown
and other metabolic reactions (removed by
breathing).
Sulfuric acid CHON breakdown
Lactic acid incomplete glucose breakdown
under anaerobic (no O2) conditions
Ketoacids incomplete breakdown of FA
(under anaerobic conditions)
MAGKARIBAL
ACIDOSIS
H K
K H
K H K
K
K K
K
H K K
K
H K
ALKALOSIS
K H K
K H
K H K H K
K K
K
H K K
K
K H
K
K
H
K
K
H K
K
H K K
H
H
H
K
K
H
Compensation
a. Excess H+ & CO2
RR CO2 pH
b. Deficient H+ & CO2
RR CO2 pH
b. Kidneys
permanently remove H+ from the body,
reabsorb acids or bases and produce HCO3
ions in the proximal tubule.
Regulates acid or base in the ECF by
excreting either acidic or alkaline urine.
Most powerful regulator of acid/base balance
Slowest response, taking hours or days to
effectively regulate the pH.
Regulation
pH increase renal absorption of HCO3
pH increase renal excretion of HCO3
TYPES OF ACID-BASE
IMBALANCES
Metabolic Acidosis
(Base HCO3 deficit < 23mEq/L)
accumulation of metabolic acids (e.g.
lactic acid & ketoacids) that rise in
proportion to HCO3 resulting in ph.
Secondary to an existing disease.
4. Underelimination of H+
Kidney and Acute/Chronic lung disease
*Kidneys: inability of the tubules to excrete
H+ into the urine
*Lungs: inability to excrete CO2
5. Underproduction of HCO3+
HCO3 is made in the kidneys, liver,
pancreas; failure cause a base-deficit
acidosis
E.g. RF, LF, Pancreatitis, Dehydration
4. Overelimination of HCO3+
loss of excessive intestinal secretions w/c has
high HCO3 concentration
Causes
diarrhea
pancreatic or biliary fistula drainage
ileostomy, intestinal suction
ileal bladder
HCO3 is lost in the urine
Metabolic Acidosis
Renal Buffering
H+ ion
excretion
HCO3
retention
NH3 NH4
production
Neurological Manifestations
Headache
manifestations
Clinical
Malaise
Weakness
Fatigue
Stupor/coma
CLINICAL MANIFESTATIONS
SNS Manifestations
Vasodilation
Warm, flushed skin, dry
Decreased skin turgor
Respiratory Manifestations
Kussmauls respirations
Fruity breath (DKA)
Gastrointestinal Manifestations
Nausea
Vomiting
Anorexia
LABORATORY RESULTS
ABG:
pH<7.35,
PaCO2 normal,
HCO3 <22mEq/L
K>5.3mEq/L
CL>106mEq/L
Lung Compensation:
increasing RR and depth of respirations
through hyperventilation moving pH to
normal
ABG: Normal pH, PaCO2, HCO3<22mEq/L
NURSING DIAGNOSES
Deficient fluid volume r/t dehydration
Risk for injury r/t skeletal muscle
weakness
Decreased cardiac output r/t poor
cardiac contractility and decreased
vascular volume.
Impaired memory r/t fluid and
electrolyte imbalances.
COLLABORATIVE MANAGEMENT
Goal
Correct the underlying problem, and
restoring fluid and electrolyte loss
increasing aerobic metabolism,
monitoring for change.
MEDICAL INTERVENTIONS
Hydration
Calcium supplement
Alkalinizing agents (HCO3 <12 mEq/L.)
Hemodialysis or peritoneal dialysis.
DKA- Insulin
Antidiarrials
NURSING MANAGEMENT
Monitor ABG levels
Maintain patent IV access
Administer drugs as ordered.
Monitor I&O
Monitor determinants of tissue O2 delivery
(e.g. PaO2, SaO2,Hgb, cardiac output)
Monitor loss of HCO3 through GIT
OFI, administer fluids
Prepare for dialysis
Institute seizure precautions.
EVALUATION
Acute/Chronic
Respiratory
Acidosis
(H2CO3 Excess)
Acute/Chronic Respiratory
Acidosis (H2CO3 Excess)
state of relative excess of acid in
body fluids resulting from retention
or excessive production of CO2.
Hypoventilation CO2 & H+
concentration in the lungs and
blood
ETIOLOGY
ACUTE CAUSES
Cardiopulmoary arrest
Pneumothorax or hydrothorax
Chest wall trauma
Acute abdominal distention
Drug overdose (sedatives, anesthesia)
Airway obstruction
Pulmonary edema/ARDS
Atelectasis
Cont. ETIOLOGY
ACUTE CAUSES
Pneumonia
Acute neurologic dysfunction from any cause
(cerebral trauma, GBS)
Sleep apnea syndrome = reduced diameter
of upper airway during sleep
Excessive O2 adm to pt with chronic
hypercapnia (excessive CO2 in the blood)
Electrolyte imbalance
Pulmonary emboli
CHRONIC CAUSES
Chronic emphysema and bronchitis
Myasthenia gravis = weakness of voluntary
muscles
Cystic fibrosis
COPD
CHF
Pulmonary fibrosis
Muscular dystrophy= progressive wasting of
the skeletal or voluntary muscles.
Respiratory Acidosis
Hypoventilation
Hypercapnia ( PaCO2)
Blood pH
Renal buffering 48-72 hrs
H+ excretion & HCO3 ret
NH3 - NH4 production
Clinical Manifestations
a. Neurological Manifestations
Headache
Blurred vision
Tremors
Muscle Twitching
Vertigo
Irritability
Disorientation
Lethargy
Coma
Cardiac Manifestations
Tachycardia
BP
Cardiac dysrhythmias
Ventricular fibrillation = first sign of
respiratory acidosis for anesthetized
patients.
Respiratory Manifestations
Initial hyperventilation
Eventual hypoventilation result to Acute hypercapnia
Acute Hypercapnia
- PR & RR BP (acute)
- more serious threat to life than acidemia or hypercapnia
- retained CO2 displaces O2 in the alveoli
- PR & RR BP (acute)
Rapid PaCO2 eg. 60 mmHg
Cerebral vasodilation
COLLABORATIVE MANAGEMENT
Medical
GOAL: Maintain patent airway and enhance gas
exchange
a. Pharmacologic agents
Bronchodilators
Mucolytics
Antibiotics
Thrombolytics or anticoagulants for pulmonary
emboli
b. O2 Rx
Ventilation support : SaO290, respiratory muscle
fatigue
c. Pulmonary hygiene: positioning, tapping, OFI
NURSING MANAGEMENT
Semi-Fowlers position
Administer low flow O2
Monitor ABG levels for changes in pH and CO2
Monitor for symptoms of respiratory failure
(PaO2, PaCO2, respiratory muscle fatigue )
Provide low CHO, high fat diet to reduce CO2
production
Monitor neurologic status (LOC, confusion)
Pulmonary hygiene Monitor V/S
Protect pt from injury
Provide emotional support and reassurance to allay
anxiety
Prevent complications : Monitor RR, and depth,
cyanosis, color of nail beds and mucous membranes for
cyanosis (late finding)
COMBINED
METABOLIC
&
RESPIRATORY
ACIDOSIS
(MIXED ACIDOSIS)
METABOLIC
ALKALOSIS
(Base HCO3 excess)
METABOLIC ALKALOSIS
Occurs when the HCO3 level rises
above the 27mEq/L and the pH
above 7.45
increased loss of acid (stomach &
kidneys)
Loss of fixed acid decreases H+
concentration
2. ACID DEFICIT
Prolonged vomiting
Nasogastric suctioning
Cushings syndrome or disease
Hyperaldosterolism
Thiazide diuretics
Pyloric stenosis
Metabolic alkalosis
Renal buffering
H retention
HCO3
excretion
Blood pH returns
to normal
Clinical Manifestations of
Met Alkalosis
METABOLIC ALKALOSIS
DIAGNOSTIC FINDINGS
ABG
ph > 7.45
PaCO2 - normal
HCO3 > 26 mEq/L/
K accompanies metabolic alkalosis
Ca Ca binding increases and the blood
level of Ca decreases
Chloride levels
Compensation: Lungs compensation RR
CO2
= pH or N; PaCO2; HCO3 (no change)
RESPIRATORY
ALKALOSIS
(H2CO3 deficit)
RESPIRATORY ALKALOSIS
(H2CO3 deficit)
relative excess of base in body fluids
resulting from respiratory elimination of
CO2.
- may be intentional as with mechanical
ventilation
- Or accidental as in panic attack
a. Alveolar hyperventilation
Acute hypoxia (early stage): PNA, BA, PE
Hypoxemia: Asphyxiation, high altitudes, shock,
pulmonary fibrosis, cyanotic heart disease
Anxiety
Fever
b. Early stages of Salicylate toxicity = cross the bloodbrain barrier & stimulate the respiratory center
causing hyperventilation
c. CNS: trauma, seizures, catecholamines,
Exercise
Gram-negative sepsis
d. Excessive mechanical ventilation and anesthesia=
intentional
Pregnancy
Respiratory
Alkalosis
Hyperventilation
Hypocapnia ( PaCO2)
Blood ph
Hypoventilation
Retention of CO2
Renal Buffering 48 72
hrs
H+retention
HCO3 exc.
Blood ph returns to
normal
Clinical Manifestation
Light-headedness and dizziness = CO2 crosses the
blood-brain barrier causing vasoconstriction and
cerebral blood flow
Inability to concentrate
Numbness & tingling around the mouth, fingers
and mouth = Ca levels 2 binding of Ca to
protein
Dysrhythmias & muscle weakness = K+ & Ca+
+
Chest pain = 2 coronary spasm
GIT: nausea, vomiting & diarrhea d/t alkalosis
Sweating, palpitation, panic, or air hunger may
also be present.
Renal Compensation
Excretion of HCO3 and
absorption of H ions.
NURSING DIAGNOSES
Ineffective breathing pattern
High risk for injury
Anxiety
Impaired memory
Fatigue
Activity intolerance
Altered thought process
COLLABORATIVE MANAGEMENT
GOAL:
a. Promotion of A/B balance
b. Prevention of complications resulting
from PaCO2 levels lower than desired.
Interventions
Encourage slow, deep breathing
Monitor ABG levels for increased pH level.
Monitor for indications of respiratory failure
(PaO2 level, respiratory muscle fatigue,SaO2
level)
Monitor for hyperventilation resulting in
respiratory alkalosis (e.g. hypoxemia, CNS injury,
hypermetabolic states, GI distention, pain, stress).
Nursing
Monitor for CP manifestations of respiratory
alkalosis (e.g. arrhythmias, cardiac output,
and hyperventilation).
Provide O2 Rx., if necessary.
Reduce O2 consumption to minimize
hyperventilation (e.g. promote comfort,
control fever, reduce anxiiety)
Provide ventilatory support, if necessary.
Assess patient for respiratory depression
Provide emotional support and reassurance
to the patient to reduce anxiety
Evaluation
ABG values return to normal
Heart rate, rhythm, and blood
pressure return to normal
The patient remains injury free.
ARTERIAL
BLOOD
ANALYSIS
ABG Interpretation
Steps
Step 1
Normal Values
pH: 7.35 7.45
paCO2: 35 45 mmHg
HCO3: 22-26/23-27 mEq/dl
paO2: 80-100%
O2 saturation : 95-100%
B. PARTIAL COMPENSATION
-Acid/base balance is compensated
and pH is still ABNORMAL.
pH
paCO2
HCO3
7.30
50
30
7.30
33
20
C. COMPLETE COMPENSATION
- Acid/base balance is compensated and pH
returns to NORMAL
pH
paCO2
HCO3
N 7.36
50
30
N 7.36
33
20
Compensation absent:
One component (PaCO2 or HCO3) is
abnormal, the other normal
Resp
Met
pH
7.33
7.33
paCO2
50
N 38
HCO3
N 24
20
pH ( 7.357.45)
PaCO2
(35-45)
HCO3
Interpretation
(22-26)
= no change in HCO3
7.20
60 mmHg
increase in HCO3 pH is
abnormally low
7.42 (N)
60 mmHg
37
mEq/L
Met ALK FC
= opposite direction; 1 is
acidotic; 1 is alkalotic;
LUNGS RETAINED CO2
moving Ph to normal
34 mmHg
24 mEq/L
(N)
Resp Alkalosis
Uncompensated
7.45
34 mmHg
20 mEq/L
Resp Alkalosis PC
= opposite direction,
1 acidotic,1 alkalotic
7.38
(N)
34 mmHg
to balance w/ lowered
acid levels, moving pH
to normal
7.30
40 mm Hg
(N)
change in PaCO2
7.30
32 mm Hg
= decrease in PaCO2
7.42 (N)
32 mm Hg
20 mEq/L
Resp Alk FC
7.46
40 mm Hg
(N)
28 mEq/L
Met Alkalosis
Uncompensated; no
change in PaCO2
7.46
48 mm Hg
28 mEq/L
7.42 (N)
48 mm Hg
7.30
50 mm Hg
20 mEq/L
Mixed Acidosis
7.48
33 mm Hg
29 mEq/L
Mixed Alkalosis
pH
PaCO2 HCO3
pH
PaCO2 HCO3
s
7.48
42
30
6.
7.26
50
21
2 7.34
.
46
24
7.
7.45
30
30
3 7.32
.
38
20
8.
7.32
32
14
4 7.61
.
21
20.6
9.
7.37
28
21
5 7.39
.
49
29.3
10. 7.38
48
29
If you fail to
prepare,
You prepared to
fail!
END