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RESPIRATORY ACIDOSIS AND

ALKALOSIS
AND
METABOLIC ACIDOSIS AND
ALKALOSIS

Dr.VINEELA
Dept of General Medicine
• Define respiratory acidosis ?
Respiratory Acidosis
• ↑ in PaCO2> 45 mmHg and pH <7.35
• due to inadequate alveolar ventilation.
• What are the cuases of acute respiratory
acidosis?
• Alveolar hypoventilation
• Increased CO2 production
Alveolar hypoventilation
• Central nervous system depression
• Neuromuscular disorders
• Chest wall abnormalities
• Pleural abnormalities
• Airway obstruction
• Parenchymal lung disease
• Ventilator malfunction
Increased CO2 production
• Large caloric loads
• Malignant hyperthermia
• Intensive shivering
• Prolonged seizure activity
• Thyroid storm
• Extensive thermal injury (burns)
• What are clinical manifestations of
respiratory acidosis?
Manifestations of Respiratory Acidosis

•Mainly NEUROMUSCULAR: CO2 narcosis

•Anxiety, Headache, Lethargy, Stupor,


Focal Paresis, Tremors, Asterixis,
Delirium, myoclonus, Seizures, Coma
• How to correct respiratory acidosis?
• By altering TV or f in mechanically
ventilated patients.

• ↑Minute Ventilation will ↓


PaCO2.

• Recommended guidelines are


to
– Target the TV 5-8 mL/kg of
(IBW)
• What are the factors that affect PaCO2
during mechanical ventilation?
• VCO2, carbon dioxide
production;
• VA, alveolarventilation;
VE , minute
ventilation; VD , dead
space ventilation;
• VT, tidal volume;
• TI, inspiratory
time; TE, expiratory
time;
• f, respiratory rate.
• Define Respiratory alkalosis ?
• PaCO2 <35 mm Hg and pH>7.45,
• due to excessive alveolar ventilation.
• What are the causes of respiratory
alkalosis?
Causes of Respiratory Alkalosis
CENTRAL RESPIRATORY STIMULATION

Structural Causes Non Structural Causes


Head trauma Pain
Brain tumor Anxiety
CVA Fever
Voluntary
PERIPHERAL RESPIRATORY STIMULATION
• Hypoxemia  Reflex Stimulation of Respiratory
Center via Peripheral Chemoreceptors
• V/Q imbalance
• Pulmonary Diffusion Defects
• Hypotension
• Pulmonary Shunt
• High Altitude
INTRATHORACIC STRUCTURAL CAUSES:
• ↓ movement of chest wall & diaphragm
• ↓ compliance of lungs
• Irritative lesions of conducting airways

OTHERS:
• Heat exposure, Sepsis, Pregnency,
Mechanical ventilation
• What are menifestation of respiratory
alkalosis?
Manifestations of Respiratory Alkalosis

• Mainly NEUROMUSCULAR:
• Lightheadedness, Confusion, Decreased
intellectual function,
• Paraesthesias (circumoral, extremities)
• Muscle twitching, cramps, tetany,
Hyperreflexia
• Syncope, Seizures
• How to correct Respiratory alkalosis in
mechanically ventilated patient?
• We have to treat Hyperventilation

• For VCV, ↓ minute ventilation by ↓ f, and


then ↓ VT if necessary .

• for PCV, decrease f first and then


decrease inspiratory pressure, if
necessary.
THANK YOU
• Define metabolic acidosis?
• primary ↓ in HCO3 (< 22 mEq/L) and pH
<7.35 .
• What are the pathophysiology of
Metabolic acidosis?
Pathophysiology
• HCO3 loss: Renal or GIT
• Decreased renal acid excretion
• Increased production of non-volatile acids
a. Ketoacids
b. Lactate
c. Poisons
d. Exogenous acids
• What are the causes of high AG
metabolic acidosis?
Causes of High AG Metabolic Acidosis
• Starvation

• Ketoacidosis: Diabetic, Alcoholic


• Lactic Acidosis

• Toxicity: Methanol, Ethylene Glycol,


Propylene Glycol, Paraldehyde, Salicylates.
• Renal Failure
• What are the causes of Non AG
metabolic acidosis?
Causes of Non AG Metabolic Acidosis
HCO3 loss:
GIT:- Diarrhoea, Pancreatic or biliary drainage,
ureterosigmoidostomy
Renal:- Proximal (type 2) RTA, Ketoacidosis (during
therapy)

Impaired renal acid excretion:


Distal (type 1) RTA, Hyperkalemia (type 4) RTA
Hypoaldosteronism, Renal Failure
Misc:
Hyperalimentation , Cholestyramine, HCl
therapy
• What are the menifestation of
metabolic acidosis?
Manifestations of Metabolic Acidosis
CARDIOVASCULAR:-
• Impaired cardiac contractility,
• ↑ pulmonary vascular resistance,
• ↓ in CO, BP & hepatic and renal Blood flow,
Sensitization to reentrant arrhythmias & reduced
threshold of VF,
• Attenuation of cardiovascular responsiveness to
catecholamines
RESPIRATORY:-
• Hyperventilation
•  strength of respiratory muscles & muscle
fatigue
•Dyspnea
CEREBRAL:-
• Inhibition
of
metabolis
METABOLIC:
• Increased metabolic demands
• Insulin resistance
• Inhibition of anaerobic glycolysis
• Reduction in ATP synthesis
• Hyperkalemia(secondary to cellular shifts)
• Increased protein degradation
• What are the management of Metabolic
acidosis?
General measures:-
• Correct Any respiratory component of the
acidemia.
• PaCO2 to be maintained (≈30) to partially
return pH to normal.
• If pH < 7.20*, NaHCO3 (usually a 7.5%
solution), may be necessary.
The amount of NaHCO3 given :
• empirically as a fixed dose (1 mEq/kg)
or
• derived from the base excess and the calculated
bicarbonate space
NaHCO3 = Base Deficit × 30% × body weight in
Kg
• Only 50% of the calculated dose is given,
after which another ABG is measured”
• Serial ABG are mandatory to avoid
complications(e.g, overshoot alkalosis and
sodium overload) and to guide further
therapy.
• pH>7.25 is sufficient to overcome the adverse
physiological effects of the acidemia.
• Profound or refractory acidemia may require
acute hemodialysis
• NaHCO3 in treating cardiac arrest and low
flow states is not recommended - Paradoxical
intracellular acidosis - particularly when CO2
elimination is impaired
• Alternate buffers that do not produce CO2 ,
such as Carbicarb or tromethamine (THAM) .
Specific therapy of Metabolic acidosis
• DKA: Replacement of the existing fluid deficit
(as a result of a hyperglycemic osmotic
diuresis) as well as insulin, potassium,
phosphate, and magnesium.
• Lactic Acidosis:- restoring adequate
oxygenation and tissue perfusion.
• Salicylate toxicity:- Alkalinization of the urine
with NaHCO3 to a pH >7.0 increases its
elimination
• Define Metabolic alkalosis?
• Primary ↑ in plasma HCO3>26mEq/L
and pH >7.45.
• What are the pathophysiology of
metabolic Alkalosis?
Pathophysiology

• HCO3- gain
• H+ loss either from Renal or from GIT
• H+ shift from ICF to ECF
• Contraction of volume/chloride depletion
• What are the causes of metabolic
alkalosis?
Chloride-sensitive
• Gastrointestinal:- Vomiting, Gastric drainage,
diarrhea
• Renal:- Diuretics
• Sweat:- Cystic fibrosis
Chloride-resistant
• Primary hyperaldosteronism
• Edematous disorders (secondary)
• Cushing’s syndrome
• Severe hypokalemia
Miscellaneous
• Massive blood transfusion
• Acetate-containing colloid solutions
• Alkaline administration with renal insufficiency
• Alkali therapy
• Combined antacid and cation-exchange resin
therapy
• Hypercalcemia
Milk-alkali syndrome
Bone metastases
• Sodium penicillins
• Glucose feeding after
starvation
• What are the menifestation of
metabolic alkalosis?
Manifestations of Metabolic Alkalosis

•Cardiovascular
Arteriolar constriction
Reduction in Coronary BF/ Anginal threshold
Predisposition to refractory SV & V arrhythmias
(especially if pH > 7.6)
•Respiratory - Hypoventilation
(Compensatory)
 Hypercapnia / Hypoxemia
• Metabolic
Stimulation of anaerobic glycolysis & organic
acid production
Reduction plasma ionized Calcium conc
Hypokalemia (secondary to cellular shifts)
Hypomagnesemia & Hypophosphatemia
• Cerebral
Reduction in Cerebral BF  mental status
changes (stupor, lethargy & delirium)
N-M irritability (related to low ionized
plasma Ca)
• What are the management of
metabolic alkalosis?
• Correction of metabolic alkalosis is never
complete until the underlying disorder is treated.
• On controlled ventilation, any respiratory
component causing alkalemia should be
corrected by ↓ MV to normalize PaCO2 .
• TOC for Cl-sensitive metabolic alkalosis -
administration of iv saline (NaCl) and potassium
(KCl).
• H2 -blocker therapy is useful when excessive loss
of gastric fluid is a factor.
• Acetazolamide may also be useful in edematous
patients.
• Alkalosis associated with primary ↑ in
mineralocorticoid activity readily responds to
aldosterone antagonists (spironolactone).
• When pH > 7.60, treatment with:
iv HCl(0.1 mol/L) , NH4Cl(0.1 mol/L) , arginine
hydrochloride,
Or
hemodialysis.
How to diagnose
ACID-BASE disoder?
Structured approach to diagnosis

First: Initial clinical assessment based on clinical


details
•From history, examination and investigations make a clinical
decision as to what is the most likely acid-base disorder

•Be aware that in some situations the history may be


inadequate, misleading or the range of possible diagnosis is
large

•Mixed disorders are always very difficult


Second: Acid – Base Diagnosis

Perform a systematic evaluation of the blood gas and


other results and make an acid-base diagnosis

Finally: Clinical Diagnosis

Synthesize the information to make an overall clinical


diagnosis
Term
s
• ACIDS • BASES
–Acidemia –Alkalemia
–Acidosis –Alkalosis
•Respiratory •Respiratory
CO2 CO2
•Metabolic •Metabolic
HCO3 HCO3
When you read an ABG which
parameter you read first?

• Oxygenation
Adequacy of Oxygen
• Look at the PaO2, SaO2 and FiO2 of patient
• Predicted minimum
– PaO2 = FiO2 x 5,
– COPD = FiO2 X 3
• Normal PaO2/FiO2 ratio:105mmHg/0.21=500,
• < 300 = ARDS(ALI included in it;Berlin criteria)
Classify pH as normal, acidemia and alkalemia

• First look at the pH – any deviation from normal


• ed pH < 7.35, Acidemia, then Uncompensated disorder
• ed pH > 7.45, Alkalemia, then Uncompensated disorder
• pH (7.35 – 7.45) – Normal, then there must be either
no disorder or a compensated disorder
Grading ACIDAEMIA ALKALAEMIA
Mild 7.30-7.34 7.46-7.50
Moderate 7.20-7.29 7.51-7.54
Severe <7.2 >7.55
Incompatible with <6.8 >7.8
life
Analyze: disorder is Respiratory or
Metabolic
• Respiratory – if pH and PaCO2 move in Opposite
direction in relation to normal values. (OR)
• Metabolic – if pH and PaCO2 move in Same
direction. (SM)
• Primary Respiratory acidosis – ↓ pH & ↑
PaCO2
• Primary Respiratory alkalosis - ↑ pH & ↓
PaCO2
• Primary Metabolic acidosis – ↓ pH and ↓
Evaluate compensation and correlate pH,
PCO2, HCO3
• With time body tries to bring pH towards normal.
• Lungs and kidneys are primary buffer response systems.
• Primary Respiratory acidosis – ↓ pH & ↑ PaCO2 ↑
HCO3
• Primary Respiratory alkalosis - ↑ pH & ↓ PaCO2 ↓
HCO3
• Primary Metabolic acidosis – ↓ pH and ↓ PaCO2 ↓
HCO3
• Primary Metabolic alkalosis –↑ pH and ↑ PaCO2 ↑
HCO3
Calculate actual compensation seen and match
with expected
• If diagnosed Primary respiratory acidosis/alkalosis –
• Is there appropriate renal compensation – Acute or Chronic
• Acute Resp Acidosis: 10 mm Hg ↑ PaCO2 above 40 = ↑HCO3 by 1
mmol/L
• Acute Resp Alkalosis: 10 mm Hg ↓ PaCO2 below 40 = ↓ HCO3 by 2
mmol/L
• Chronic Resp Acidosis: 10 mm Hg ↑ PaCO2 above 40 = ↑HCO3 by 3
mmol/L
• Chronic Resp Alkalosis: 10 mm Hg ↓ PaCO2 below 40 = ↓HCO3 by
4 mmol/L OR
• Rise of PaCO2 by 20 mmHg = fall of pH by 0.1
• Fall of PaCO2 by 10 mmHg = rise of pH by 0.1
Calculate actual compensation seen and match with expected

• If diagnosed Primary Metabolic acidosis/alkalosis


• Look for the expected change in PaCO2 –
• If PaCO2 is Higher, or Lower than that expected –
then
• With a primary metabolic disorder a superimposed
primary respiratory disorder is present
Expected change in PaCO2
• Metabolic acidosis - Expected Compensation in
PaCO2 = 1.5 x HCO3+ 8 (±2)
• Metabolic alkalosis - Expected compensation in
PaCO2 = 0.7 × HCO3+ 21 (±2)
Find out if the disorder is mixed

• If pH is normal – And PaCO2 – is High or Low


• Normal pH with High PaCO2 indicates a Mixed
Respiratory Acidosis & Metabolic Alkalosis
• Normal pH with Low PaCO2 indicates a Mixed
Respiratory Alkalosis & Metabolic Acidosis
• Therefore, if the PaCO2 is 70 mm Hg and the pH is 7.40,
the compensatory change in pH is more than expected
indicating that there is metabolic alkalosis in addition to
the compensation .
Unmask hidden disorders

• If Metabolic Acidosis is diagnosed – Check Anion Gap


• To assess the associated metabolic disorder and also
explain the cause of metabolic acidosis

• Δ AG/ Δ HCO3 < 0.1 - Combined high AG acidosis +


non AG acidosis
• Δ AG/ Δ HCO3 = 1 - Anion Gap acidosis, DKA
due to urinary ketone loss
• Δ AG/ Δ HCO3 >1.5 Metabolic acidosis and
alkalosis
Points to remember

RESPIRATORY ACIDOSIS:
• Primary change is ↑ in PaCO2 leading to a ↓ in pH
• For each 10 mm Hg ↑ in PaCO2, pH ↓ by 0.05

RESPIRATORY ALKALOSIS:
• Primary change is ↓ in PaCO2 leading to ↑ in pH
• For each 10 mm Hg ↓ in PaCO2 pH ↑ by 0.1
Points to remember

METABOLIC ACIDOSIS:
• Primary change is ↓ in HCO3 or ↑ H+ leading to ↓ pH
• For ↓ in HCO3 of 7 – 7.5 mEq/ L, pH ↓ by 0.1

METABOLIC ALKALOSIS:
• Primary change is ↑ HCO3 or ↓ H+ leading to ↑ pH
• For ↑ in HCO3 of 7-7.5 mEq/L - pH ↑ by 0.1

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