Acid Base Disturbances Acidosis Alkalosis Type Of Disturbances Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

1. Be Confident…!!!!
Acid – Base Disturbances
Acid–base imbalance is an abnormality of the human body's normal balance of acids and bases that
causes the plasma pH to deviate out of the normal range (7.35 to 7.45).
Ordinarily, chemical and physiological buffer systems maintain the hydrogen ion concentration of body
fluids within very narrow pH ranges. Abnormal conditions may disturb the acid-base balance. For
example:
 The pH of arterial blood is normally 7.35-7.45.
 A pH value below 7.35 produces Acidosis.
 A pH above 7.45 produces Alkalosis.
Such shifts in the pH of body fluids may be life threatening. In fact,a person usually cannot survive if the
pH drops to 6.8 or rises to 8.0 for more than a few hours.
ACIDOSIS
Acidosis results from an accumulation of acids or a loss of bases,both of which cause abnormal increases
in the hydrogen ion concentrations of body fluids.

2. ALKALOSIS
Alkalosis results from a loss of acids or an accumulation of bases accompanied by a decrease in hydrogen
ion concentrations.
TYPES OF DISTRUBANCES
There Are Four BasicTypesof Imbalance/Disturbances:
1. Respiratory Acidosis
2. Respiratory Alkalosis
3. MetabolicAcidosis
4. MetabolicAlkalosis
If PaCO2 primarily ↑, pH tends to be ↓— Respiratory Acidosis
If PaCO2 primarily ↓, pH tends to be ↑— Respiratory Alkalosis
If [HCO3
-] primarily ↓, pH tends to be ↓— Metabolic Acidosis
If [HCO3
-
] primarily ↑, pH tends to be ↑— Metabolic Alkalosis
Respiratory Acidosis

3.  Respiratoryacidosisisaconditioninwhichabuild-upof carbondioxide inthe bloodproducesa
shiftinthe body'spH balance and causesthe body'ssystemto become more acidic.
 Thisconditionisbroughtaboutby a problemeitherinvolvingthe lungsandrespiratorysystem
or signalsfromthe brainthat control breathing.
 There isprimaryincrease inPco2 withcompensatoryincrease inHCO3−; pH usuallylow but
may be near normal.(Ventilatoryfailure;Respiratoryfailure;Acidosis –respiratory)
Mechanism:
 Carbondioxide isproducedconstantlyasthe bodyburnsenergy,andthisCO2will accumulate
rapidlyif the lungsdonot adequatelydispelitthroughalveolarventilation.
 AlveolarhypoventilationthusleadstoanincreasedPaCO2(called Hypercapnia).The increase in
PaCO2 inturn decreasesthe HCO3−/PaCO2ratio anddecreasespHresultingrespiratory
acidosis.
Types of Respiratory Acidosis:

4. 1- Acute Respiratory Acidosis
2- Chronic Respiratory Acidosis
1. Acute Respiratory Acidosis:
 Acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range
(over 6.3 kPa or 47 mm Hg) with an accompanying Acidemia (pH <7.35).
 Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in
ventilation may be caused by:
 Depression of the central respiratory center by cerebraldisease or drugs.
 Inability to ventilate adequately due to neuromuscular disease (e.g.,myasthenia
gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy).
 Airway obstruction related to asthma or chronic obstructive pulmonary disease
(COPD) exacerbation.
2. Chronic Respiratory Acidosis:
 Chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference
range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal
compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg).
 Chronic respiratory acidosis may be secondary to many disorders, including COPD.
 Hypoventilation in COPD involves multiple mechanisms, including
 Decreased responsiveness to hypoxia and Hypercapnia
 Increased ventilation-perfusion mismatch leading to increased dead space ventilation
 Decreased diaphragm function secondary to fatigue and hyperinflatio
 Chronic respiratory acidosis also may be secondary to:
 Obesity hypoventilation syndrome (i.e., Pickwickian syndrome)
 Neuromuscular disorders such as amyotrophic lateral sclerosis
 Severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic
deformities
Causes:
 Hypoventilation
 Diseasesof the airways(suchasasthma and chronic obstructive lung disease),whichsendair
intoand outof the lungs
 Diseasesof the chest(suchas scoliosis),whichmake the lungslessefficientatfillingand
emptying
 Diseasesaffectingthe nervesandmusclesthat"signal"the lungsto inflate ordeflate
 Drugs that suppressbreathing(includingpowerful painmedicines,suchasnarcotics,and
"downers,"suchasbenzodiazepines),especiallywhencombinedwithalcohol
 Severe obesity,whichrestrictshow manythe lungs, canexpand.

5. Signs and Symptoms:
Sign And Symptoms of Respiratory Acidosis
Central Nervous System Respiratory System Cardiovascular System
 Mildand moderate
Hypercapnia
 Cerebral
Vasodilatation
 IncreasedIntracranial
Pressure
 Headache
 Confusion
 Hallucinations
 TransientPsychosis
 MyoclonicJerks
 FlappingTremor
 Severe Hypercapnia
 Stupor
 Coma
 ConstrictedPupils
 DepressedTendon
Reflexes
 ExtensorPlantar
Response
 Seizures
 Breathlessness
 Central andPeripheral
Cyanosis
 PulmonaryHypertension
 Mildto moderate Hypercapnia
 Warm and Flushed
skin
 BoundingPulse
 Well maintained
Cardiac outputand
bloodpressure
 Diaphoresis
 Severe Hypercapnia
 Cor Pulmonale
 DecreasedCardiac
output
 SystemicHypotension
 Cardiac Arrhythmias
 Pre-renal Azotemia
 Peripheral Edema

6.  Papilledema
Compensation:
 Problem: Increase pCO2 and these results in a decrease blood pH (high H+)
 [H+] stimulates kidney to generate and retain bicarbonate
 Respiratory acidosis is compensated for by the development of a metabolic
alkalosis
 Compensation is complete ([HCO3] levels out) in 2-4 days
 Final HCO3 can be calculated from the following equation:
 HCO3 mmol/L = 0.44 X pCO2 mmHg + 7.6 (+/-2).
 Limit of compensation is a HCO3 of 45 mmol/L
Alteration of Metabolism and Function:
• Also include dysfunction of cardiovascular system and CNS.
• Respiratory acidosis usually has more profound impacts on CNS than metabolic acidosis with the
same plasma pH
– CO2 readily across blood-brain-barrier, and elevated level of CO2 can make
vasodilatation of cerebralblood vessel→↑ cerebralblood volume and intracranial
pressure
– HCO3
-
is water-soluble, and cannot pass through blood-brain-barrier as easy as CO2→ the
pH value of cerebrospinal fluid in respiratory acidosis is usually lower than that of
metabolic acidosis
RESPIRATORY ALKALOSIS
Respiratory alkalosis is a condition where the amount of carbon dioxide found in the blood drops to a
level below normal range. This condition produces a shift in the body's pH balance and causes the body's
system to become more alkaline (basic). This condition is brought on by rapid, deep breathing called

7. hyperventilation. There is a primary decrease in Pco2 with or without compensatory decrease in HCO3 −
pH high or near normal. (Alkalosis – respiratory)
Mechanism:
Respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased
breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the
dynamic chemical equilibrium of carbon dioxide in the circulatory system, and the system reacts
according to Le Chatelier's principle. Circulating hydrogen ions and bicarbonate are shifted through the
carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase .The net
result of this is decreased circulating hydrogen ion concentration, and thus increased pH (alkalosis). There
is also a decrease in ionized blood calcium concentration.
Types of Respiratory Alkalosis:
1. Acute Respiratory Alkalosis:
 It occurs rapidly.
 During acute respiratory alkalosis, the person may lose consciousness where the rate of
ventilation will resume to normal.
2. Chronic Respiratory Alkalosis:
 It is a more long-standing condition.
 For every 10 mM drop in pCO2 in blood, there is a corresponding 5 mM of bicarbonate
ion drop. The drop of 5 mM of bicarbonate ion is a compensation effect which reduces
the alkalosis effect of the drop in pCO2 in blood. This is termed metabolic compensation.
Causes:
 Hyperventilation

8.  Intracerebral hemorrhage,meningitis,stroke
 Salicylate andProgesterone drugusage
 Anxiety,hysteria,stressandpain
 Cirrhosisof the liver
 Sepsis
 Elevatedbodytemperature
 sexual activity,whichmayinduce excessive breathingdue toexcitation
 Hypoxia
Any lung disease that leads to shortness of breath can also cause respiratory alkalosis.
Sign and Symptoms:
SIGN AND SYMPTOMS OF RESPIRATORY ALKALOSIS
Central Nervous System Cardiovascular System Neuromuscular System
 Cerebralvasoconstriction
 Reduction in intracranial
pressure
 Light-headedness
 Confusion
 Increased deep tendon
reflexes
 Generalized seizures
 Chest oppression
 Angina pectoris
 Ischemic
electrocardiographic changes
 Normal or decreased blood
pressure
 Cardiac arrhythmias
 Peripheral vasoconstriction
 Numbness and paresthesias
of the extremities
 Circumoral numbness
 Laryngeal spasm
 Manifestations of tetany
 Muscle cramps
 Carpopedal spasm
 Trousseau’s sign

9.  Chvostek’s sign
Compensation:
 Problem:decrease pCO2causingincrease bloodpH(low H+)
 Increase pH stimulatesthe kidneytoexcretebicarbonate
o respiratoryalkalosisiscompensatedforbythe developmentof ametabolicacidosis
 If the conditionhasbeenpresentfor7days or more full compensationmayoccur.
 Compensationiscomplete ([HCO3] levelsout) in7-10days.
 The limitof compensationisaHCO3 of 12 mmol/L
Alteration of Metabolism and Function:
• Similar to that of metabolic alkalosis
• Respiratory alkalosis usually has more profound impacts on CNS than metabolic alkalosis with
the same plasma pH
– The decrease in CO2 content of blood causes constriction of cerebralblood vessel→↓
cerebralblood volume and regional cerebralischemia
METABOLIC ACIDOSIS
Metabolic acidosis results from all conditions that decrease the pH of the body fluids below 7.35, with the
exception of conditions resulting from altered function of the respiratory system.
Mechanism:

10. As hydrogen ions accumulate in the body fluids, buffers first resist a decline in pH. If the buffers cannot
compensate for the increase in hydrogen ions, the respiratory center helps regulate the body fluid pH. The
reduced pH stimulates the respiratory center,which causes hyperventilation. During hyperventilation,
carbon dioxide is eliminated at a greater rate. The elimination of carbon dioxide also eliminates excess
hydrogen ions and helps maintain the pH of the body fluids within a normal range.
If metabolic acidosis persists for many hours and if the kidneys are functional, the kidneys can also help
compensate for metabolic acidosis. They begin to secrete hydrogen ions at a greater rate and increase the
rate of bicarbonate ion reabsorption. Symptoms of metabolic acidosis appear if the respiratory and renal
systems are not able to maintain the pH of the body fluids within its normal range.
Causes:
• Central change: ↓ [HCO3
-
]
1. Direct excessive loss of HCO3
-
:
i. Diarrhea, intestinal suction or intestinal or biliary fistula
ii. Proximal renal tubular acidosis
a. caused by impaired reabsorption of HCO3
-
in the proximal tubule
iii. Treatment with carbonic anhydrase inhibitor
2. Indirect loss of HCO3
-
for buffering increased nonvolatile acid
i. Excessive intake of nonvolatile acid:
a. acetylsalicylic acid (aspirin)
b. Methanol
c. Ammonium chloride
ii. Excessive production of nonvolatile acid:
a. Lactic acidosis
 Hypoxia
 Shock, cardiac arrest,severe anemia, pulmonary edema, carbon
monoxide poisoning
 Severe liver dysfunction
b. Ketoacidosis
 Diabetes
 alcoholism
 Fasting and starvation
iii. Decreased renalexcretion of acid:
a. Renal dysfunction
b. Distal renal tubular acidosis
 caused by reduced H+
secretion in the distal nephron
Types of Metabolic Acidosis:
1. Increased AGtype
 Caused by increased nonvolatile acids, but the fixed acids containing chloride are
excluded.
2. Normal AG type
 Direct loss of HCO3-

11.  Excessive intake of acidic salt containing chloride
Sign And Symptoms:
SIGNS AND SYMPTOMS OF METABOLIC ACIDOSIS
Respiratory
System
Cardiovascular
System
Metabolism Central
Nervous
System
Skeleton
 Respiratory
distress
and dyspnea
 Decreased
strength
of respiratory
muscles and
promotion of
muscle fatigue
 Impairment of
cardiac
contractility,
arteriolar
dilation,
vasoconstriction
 Reductions in
cardiac
output, arterial
blood
pressure,and
hepatic
and renal blood
flow
 Sensitization to
reentrant
arrhythmias and
reduction
in threshold for
ventricular
fibrillation
 Increased
sympathetic
discharge but
attenuation of
cardiovascular
responsiveness
to catecholamines
 Increased
metabolic
demands
 Insulin
resistance
 Inhibition of
anaerobic
glycolysis
 Reduction in
adenosine
triphosphate
synthesis
 Hyperkalemia
 Increased
protein
degradation
 Impaired
metabolism
 Inhibition of
cell
volume
regulation
 Progressive
obtundation
 Coma
 Osteomalacia
 Fractures
Compensation:
Blood buffering:
 Increased H+
is combined immediately by the base salt of bicarbonate and non-bicarbonate buffer
system
H+
+HCO3
-
→H2CO3→CO2+H2O

12. Respiratory regulation:
 ↑[H+
] → stimulate peripheral chemoreceptor in carotid and aortic body → respiratory center
excitation → hyperpnea →↑CO2 elimination and ↓PaCO2 → [HCO3
-
] /[H2CO3] near 20/1 → pH
is maintained
 i.e. pH 7.4→7.0,
o alveolar ventilation 4L/min→30L/min
Intracellular buffering:
 ↑ [H+
] in ECF→ H+
move in cells through H+
-K+
exchange and K+
move out of cells→
hyperkalemia is resulted in
Renal regulation:
 ↑ [H+
] in ECF→ ↑activity of carbonic anhydrase, H+
-ATPase and glutaminase
– ↑Renal tubular secretion of H+
– ↑Renal tubular reaborption of HCO3
-
– ↑Renal tubular secretion of ammonia (3-5days)
Alteration of Metabolism and Function:
1. Cardiovascular System:
 Effects of acidosis on myocardial contractility:
a. H+
inhibits cardiac contractility
i. Competitively inhibits Ca2+
combine with troponin in myocardial excitation-
contraction coupling process
ii. Inhibits Ca2+
influx across the cell membrane
b. When pH = 7.2, above two opposite effect nearly equal→ no marked change of
myocardial contractility
c. When pH < 7.2, the heart less responsive to catecholamine →↓myocardial
contractility
 Effect of acidosis on vascular system:
a. H+
dilates capacitance and resistance vasculature,plus the impaired cardiac
contractility, hypotension commonly occurs.
 Arrhythmia
2. CNS: Depression
 Manifestation: weakness,Conscious disturbance, stupor, lethargy and even coma.
 Mechanism:
i. Acidosis make elevated activity of glutamate decarboxylase→↑gamma-amino
butyric acid (GABA) production, an inhibitive neurotransmitter

13. ii. Acidosis makes decreased activity of biological oxidases in
mitochondria→↓ATP production in brain.
METABOLIC ALKOLOSIS
Metabolic alkalosis refers to primary increase in plasma HCO3
-
concentration, the pH tends to be
increased.
Causes:
Central change: ↑ [HCO3
-
]:
• Excessive gain ofHCO3
-
:
 Excessive ingestion of NaHCO3
 Infusion of large amounts of stocked blood (full of citrate)
• Excessive loss ofH+
:
 excessive loss of H+
via stomach
o Vomiting, gastric suction
 excessive loss of H+
via kidney
o Aldosteronism(↑ADS), cushing’s syndrome (↑glucocorticoid)
o Thiazide and loop diuretics
 hypokalemia
• Volume contraction:
 Volume contraction→plasma HCO3
-
concentrated → contraction alkalosis
 Loss of body fluid
 Diuretic therapy
Sign and Symptoms:
SIGNS AND SYMPTOMS OF METABOLIC
Central
Nervous System
 Headache,Lethargy, Stupor
 Delirium, Tetany, Seizures
 Potentiation of hepatic encephalopathy
Cardiovascular System
 Supraventricular and ventricular arrhythmias
 Potentiation of digitalis toxicity
 Positive inotropic ventricular effect
Respiratory System  Hypoventilation with attendant Hypercapnia and hypoxemia
Neuromuscular System
 Chvostek’s sign, Trousseau’s sign
 Weakness (severity depends on degree of potassium depletion)
Metabolic Effects
 Increased organic acid and ammonia production
 Hypokalemia, Hypocalcemia, Hypomagnesemia
 Hypophosphatemia
Renal (Associated
Potassium Depletion)
 Polyuria, Polydipsia
 Urinary concentration defect
 Cortical and medullary renal cysts
Compensation:

14. • Blood buffering
– During metabolic alkalosis, ↓[H+
]ECF and ↑ [OH-
]ECF→ OH-
can be buffered by weak
acids, such as H2CO3→↑ [HCO3
-
]
• Ion exchange between intra- and extra-cell
– In alkalosis, ↓[H+
]ECF →through H+
- K+
exchange, H+
shift out of cells and K+
shift into
cells→hypokalemia
• Respiratory regulation
– ↓[H+
] →inhibition of respiratory center →↓alveolar ventilation→ ↑PaCO2 or [H2CO3] →
[HCO3
-
]/ [H2CO3] approach 20/1
– Respiratory regulation is limited and seldom make complete compensation
• ↓Alveolar ventilation → ↑ PaCO2 →but when PaCO2 >60mmHg, respiratory
center is excited→respiration deepen and quicken→↑CO2 expiration
 so compensatory limit of secondary increase of PaCO2 is 55mmHg
• Renal regulation
– ↓[H+
] → ↓the activity of carbonic anhydrase and glutaminase in renal tubular cell → ↓
renal secretion of H+
and ammonia, ↓renal reabsorption of HCO3-
→↓ [HCO3-
] in
plasma→ [HCO3
-
]/ [H2CO3] approach 20/1
– The increased renal excretion of HCO3-
peaks at 3-5 days, so this regulation is not useful
for acute metabolic alkalosis.
Alteration of Metabolism and Function:
• Mild metabolic alkalosis—asymptomatic or manifestation unrelated with alkalosis
• Severe metabolic alkalosis—many alterations of metabolism and function
1. Dysfunction of CNS: Hyperexcitability
 Manifestation: Dysphoria, mental confusion
 Mechanism:
– ↑pH→↑the activity of gamma-aminobutyric acid transaminase
(↑decomposition of GABA) and ↓the activity of glutamate decarboxylase
(↓production of GABA)→↓GABA( a inhibitory neurotransmitter) →
hyperexcitability of CNS
– ↑pH→ left-shift of oxygen-Hb dissociation→cerebral hypoxia

15. 2. Left-shift of oxygen-Hb dissociation:
 Left-shift of oxygen-Hb dissociation curve→ O2 saturation of Hb increase at
the same PaO2→releasing of O2 bound by Hb in tissue decrease → tissue
hypoxia is resulted in.
3. Hypocalcemia:
 Manifestation: tetany, carpopedal spasm, convulsion
 Mechnism:
o Free Ca2+
+ abumin combined ca2+
4. Hypokalemia:
 Mechanism
o alkalosis→H+
shift out of cells and K+
shift into cells through H+
-K+
exchange
o alkalosis→↓renal excretion of H+
and ↑renal excretion of K+
References:
1- http://www.mhhe.com/biosci/ap/foxhumphys/student/olc/u-reading5.html
2- http://www.authorstream.com/Presentation/ADahal-400878-respiratory-acidosis-alkalosis-
education-ppt-powerpoint/
3- file:///C:/Users/Nayyab/Downloads/Documents/adk1_06.pdf