ACID - BASE

IMBALANCE

Dr Simoonga Peter
 Arterial Blood Gases (ABG)
Normal values at sea level
• pH 7.35-7.45 • ↓pH - Acidosis

• PaO2 >70 mmHg • ↑pH - Alkalosis

• PaCO2 35-45 mmHg • ↓ PaO2 - Hypoxemia

• HCO3 22-28
• ↑PaCO2 -
mmol/l
Hypercapnia
 Acid–Base Balance Disturbances
Disorder pH [H+] Primary Compensatory
disturbance response
Metabolic ↓ ↑ ↓ [HCO3-] ↓ pCO2
acidosis

Metabolic ↑ ↓ ↑ [HCO3-] ↑pCO2

alkalosis

Respiratory ↓ ↑ ↑pCO2 ↑ [HCO3-]

acidosis

Respiratory ↑ ↓ ↓ pCO2 ↓ [HCO3-]

alkalosis
 Metabolic Acidosis
ANION GAP CONCEPT
• Primary AB • To know if Metabolic
disorder Acidosis due to
Loss of bicarbonate
• ↓HCO₃⁻ → ↓ pH Accumulation of non-
volatile acids
• Gain of strong
• Provides an index of the
acid relative conc of plasma
anions other than chloride,
• Loss of base bicarbonate
(HCO₃⁻) AG = [serum Na⁺ - (serum Cl⁻
+ serum HCO₃⁻)]
• Normal AG = 12mEq/L
 CAUSES OF METABOLIC ACIDOSIS
(High anion gap)→(Normochloremic)
• TOXINS
• LACTIC ACIDOSIS
Ethylene glycol
• KETOACIDOSIS
Diabetic Methanol
Alcoholic
Starvation Salicylates

• RENAL FAILURE Propylene glycol

(acute and chronic)
 Normal anion gap(Hyperchloremic)
MET.ACIDOSIS causes
Gastrointestinal
bicarbonate loss Renal acidosis
A.Diarrhea
B.External pancreatic or A. Hypokalemic
small-bowel drainage Associated with
C.Ureterosigmoidostomy,
jejunal loop, ileal loop renal tubular
acidosis (RTA)
D.Drugs
1. Calcium chloride
(acidifying agent) B. Hyperkalemic
2. Magnesium sulfate
(diarrhea)
3. Cholestyramine (bile
acid diarrhea)
 Metabolic acidosis
• Symptoms are as a • CNS:
result of the underlying Lethargy
pathology
Disorientation
• Respiratory effects: Stupor
 Hyperventilation
muscle twitching,
• CVS: COMA
 ↓ myocardial contractility CN palsies
 Sympathetic over activity
 Resistant to •Others :hyperkalemia
catecholamines
 Metabolic Alkalosis
• ↑ pH due to ↑HCO₃⁻ or ↓acid

• Initiation process :
– ↑in serum HCO₃⁻
– Excessive secretion of net daily production of
fixed acids
• Maintenance:
– ↓HCO₃⁻ excretion or ↑ HCO₃⁻ reclamation
Chloride depletion
Pottasium depletion
ECF volume depletion
CAUSES
III. Renal origin
 Exogenous HCO3 −
loads: 1. Diuretics
 Acute alkali 2. Posthypercapnic state
administration 3. Hypercalcemia /
 Milk-alkali syndrome hypoparathyroidism
4. Recovery from lactic
 Gastrointestinal origin acidosis or
 Vomiting ketoacidosis
5. Nonreabsorbable
 Gastric aspiration anions including
 Congenital penicillin, carbenicillin
chloridorrhea 6. Mg2+ deficiency
 Villous adenoma 7. K+ depletion
Metabolic Alkalosis Clinical Features
CVS Resp System
•Decreased myocardial •Hypoventilation
contractility
pulmonary micro
•Arrythmias
atelectasis
CNS V/Q mismatch
•↓ cerebral blood flow
•Confusion
•Mental obtundation
•Neuromuscular excitability
 Respiratory Acidosis
CAUSES
• ↑ PCO₂ → • CNS DEPRESSION
↓pH  DRUGS:Opiates,sedatives,anaestheti
cs
 OBESITY HYPOVENTILATION
SYNDROME
• Acute(< 24  STROKE
hours) • NEUROMUSCULAR DISORDERS
 NEUROLOGIC: MS ,POLIO, GBS,
TETANUS, BOTULISM,

• Chronic(>24  HIGH CORD LESIONS

 END PLATE:OP POISONING
hours  MUSCLE: MUSCULAR DYSTROPHY
RESPIRATORY ACIDOSIS - CAUSES
 AIRWAY  SEVERE PULMONARY
OBSTRUCTION RESTRICTIVE DISORDERS
 COPD,ACUTE  PULMONARY FIBROSIS
ASPIRATION,  PARENCHYMAL INFILTRATION:
LARYNGOSPASM Pneumonia, edema

 CHEST WALL  ABNORMAL BLOOD CO₂

RESTRICTION TRANSPORT
 PLEURAL: Effusions,  DECREASED PERFUSION:
empyema, HF,cardiac arrest,PE
pneumothorax,  SEVERE ANEMIA
fibrothorax
 ACETAZOLAMIDE-CA Inhibition
 CHEST WALL:
 RED CELL ANION EXCHANGE:
Kyphoscoliosis,
scleroderma, ankylosing Loop diuretics, salicylates, NSAID
spondylitis, obesity
Respiratory Acidosis - Clinical Features
• RS: • CVS:
 Stimulation of ventilation ( Tachycardia
tachypnea)
bounding pulse
 Dyspnea

• CNS:
 ↑cerebral blood flow→ ↑ICP • Others:
 CO₂ NARCOSIS - peripheral
(Disorientation,confusion,he
adache,lethargy)
vasodilatation
 COMA(arterial warm,
hypoxemia,↑ICT,anaesthetic flushed,
effect of ↑ PCO₂ >
sweaty
100mmHg)
 Respiratory Alkalosis
Most common AB abnormality in
critically ill patients
↓PCO₂ → ↑pH
1⁰ process : hyperventilation
Acute: PaCO₂ ↓,pH-alkalemic
Chronic: PaCO₂↓,pH normal / near
normal
CAUSES OF RESPIRATORY ALKALOSIS
• A. Central nervous • B. Hypoxemia or
system stimulation tissue hypoxia
1. Pain
1. High altitude
2. Anxiety, psychosis
3. Fever
4. Cerebrovascular 2. Septicemia
accident
5. Meningitis,
encephalitis 3. Hypotension
6. Tumor
7. Trauma 4. Severe anemia
CAUSES OF RESPIRATORY ALKALOSIS
C. Drugs or hormones
1. Pregnancy, E. Miscellaneous
progesterone 1. Septicemia
2. Salicylates
2. Hepatic failure
3. Cardiac failure
3. Mechanical
D. Stimulation of chest ventilation
receptors
4. Heat exposure
1. Hemothorax
2. Flail chest
5. Recovery from
3. Cardiac failure
metabolic
4. Pulmonary embolism
acidosis
Respiratory alkalosis Clinical Features
• CNS: • CVS:
 ↑ neuromuscular  CO& SBP ↑ (↑ SVR,HR)
irritability(tingling,ci  Arrythmias
rcumoral  ↓ myocardial contractility
numbness)
 Tetany • Others:
 ↓ ICT(cerebral VC)  Hypokalemia,hypophosp
hatemia
 ↓CBF(4% ↓ CBF
per mmHg ↓PCO₂)  Free serum calcium
 Light headedness  Hyponatremia
 confusion  hypochloremia
Respiratory Failure (RF)
(PATHOPHYSIOLOGY)

Dr Simoonga Peter
Respiratory Failure (RF)
 Definitions

 Clinical conditions in which PaO2 < 60 mmHg

while breathing room air or a PaCO2 > 50 mmHg

 Failure of oxygenation and carbon dioxide

elimination
Distinction between Acute and Chronic RF

 Acute RF  Chronic RF
 Develops over minutes to  Develops over days
hours  ↑ in HCO3
 ↓ pH quickly to <7.2  ↓ pH slightly
 Example; Pneumonia  Polycythemia, Corpulmonale
 Example; COPD
Pathophysiologic causes of RF

●Hypoventilation

●V/Q mismatch

●Shunt

●Diffusion abnormality
Pathophysiologic causes of RF
1 - Hypoventilation
 Occurs when ventilation ↓ 4-6 l/min
 Causes
 Depression of CNS from drugs
 Neuromuscular disease of respiratory ms
 ↑PaCO2 and ↓PaO2
 Alveolar –arterial PO2 gradient is normal
 COPD
Pathophysiologic causes of RF
2 -V/Q mismatch
 Most common cause of hypoxemia
 Low V/Q ratio, may occur either from
 Decrease of ventilation 2ry to airway or interstitial
lung disease
 Overperfusion in the presence of normal
ventilation e.g. PE
 Admin. of 100% O2 eliminate hypoxemia
Pathophysiologic causes of RF
3 -Shunt
 The deoxygenated blood
bypasses the ventilated
alveoli and mixes with
oxygenated blood →
Causes of Shunt
 Intracardiac
 Right to left shunt
 Fallot’s tetralogy

hypoxemia  Eisenmenger’s

 Persistent of hypoxemia
despite 100% O2 inhalation
 Hypercapnia occur when
shunt is excessive > 60%
syndrome
 Pulmonary
 A/V malformation
 Pneumonia
 Pulmonary edema
 Atelectasis/collapse
 Pulmonary contusion
Pathophysiologic causes of RF
4 - Diffusion abnormality

 Less common
 Due to
 abnormality of the alveolar membrane
 ↓ the number of the alveoli
 Causes
 ARDS
 Fibrotic lung disease
 Diagnosis of RF
1 – Clinical (symptoms, signs)
 Hypoxemia  Hypercapnia
 Dyspnea, Cyanosis  ↑Cerebral blood flow, and
 Confusion, somnolence, fits CSF Pressure
 Tachycardia, arrhythmia  Headache
 Tachypnea (good sign)  Asterixis
 Use of accessory ms  Papilloedema
 Nasal flaring  Warm extremities,
 Recession of intercostal ms collapsing pulse
 Acidosis (respiratory, and
 Polycythemia
metabolic)
 Pulmonary HTN,
 ↓pH, ↑ lactic acid
Corpulmonale, Rt. HF
Diagnosis of RF
3 - Investigations
 ABG
 CBC, Hb
 Anemia → tissue hypoxemia
 Polycythemia → chronic RF
 Urea, Creatinine
 LFT → clues to RF or its
complications
 Electrolytes (K, Mg, Ph) → Aggravate RF
 ↑ CPK, ↑ Troponin 1 → MI
 ↑CPK, normal Troponin 1 → Myositis
 TSH → Hypothyroidism
Diagnosis of RF
3 - Investigations
 Chest x ray → Pulmonary edema → ARDS
 Echocardiography → Cardiogenic pulmonary
edema
→ ARDS
→ PAP, Rt ventricular hypertrophy in CRF
■ PFT- (FEV1/ FVC ratio)
Decrease → Airflow obstruction
Increase → Restrictive lung disease
Diagnosis of RF
3 - Investigations
 ECG → cardiac cause of RF
→ Arrhythmia due to hypoxemia and
severe acidosis

■ Right heart catheterization to measure

●Pulmonary capillary wedge pressure (PCWP)
● Normal → ARDS (<18 mmHg)
● Increased → Cardiogenic pulmonary
edema
THE END
DR PETER SIMOONGA