الرحمن الله بسمالرحيم

Acid- bas balance

The power of hydrogen

Reasons for confusion

1. Why not in mmol, mEq, or mg?

2. Does the letter p of pH mean partial pressure as with pCo2 and pO2?

3. Why in acidosis when H+ increases, the pH decreases ?

The power of hydrogenH+ is kept at a very low level compared with other ions.

In a liter of pure water at 25 o C the number of moles of H+ is about 0.0000001, this is written as 1 x 10-7.

The superscript -7 is the power, the exponent or the logarithm.

The pH (or the power of hydrogen) is the negative logarithm of H+ concentration .

40 nmol/L = 0.0000004 mol/L = 10-7.4 the pH is 7.4

Body water Major body constituent.Physical properties will

affect homeostasis.Water ionizes

spontaneously into hydrogen and hydroxyl ions.

Neutral water• H+ = OH

_ = 10 -7

• pH is 7Alkaline if pH > 7Acidic if pH <7

Acids and bases

The hydrogen ion

A single highly reactive positive charge.

Why is hydrogen ion so significant?

Protein structure- function.

Ionic and hydrogen bonding will determine the final morphology.

Why is hydrogen ion so significant?pH influences:

1. Function of all enzymes.

2. Normal electrolyte distribution.

3. Myocardial performance (contractility).

4. Hemoglobin function.

H+ production1 Metabolic acids

lactate, phosphate, sulphate, acetoacetate or b-hydroxy-butyrate

Non-volatile.

Must be metabolized and excreted in urine.

40-80 mmol/day H+ load.

1 Respiratory acids

Carbonic acid

Volatile, very efficient lung excretion

CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

15,000 mmol/day H+ load.

REGULATION OF HYDROGEN ION CONCENTRATION

H + homeostasis is essential for life.Normal pH 7.35-7.45Compatible with life 6.8-8

Three systems for hydrogen homeostasis :

Chemical buffering (immediate). Respiratory compensation (hours). Renal compensation (2-4 days).

REGULATION OF HYDROGEN ION CONCENTRATION-BUFFER SYSTEM

Simple chemical neutralization.The first line of defense.A weak acid and its associate base.

1. Bicarbonate-carbonic acid system2. Plasma proteins3. Hemoglobin

REGULATION OF HYDROGEN ION CONCENTRATION-BUFFER SYSTEM-Bicarbonate –carbonic acid system

CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

REGULATION OF HYDROGEN ION CONCENTRATION-BUFFER SYSTEM-Bicarbonate –carbonic acid system

CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

REGULATION OF HYDROGEN ION CONCENTRATION- RESPIRATORY COMPENSATION

The respiratory system forms the single most important

organ system involved in the control of H+ concentration.

PaCO2 is inversely proportional to alveolar ventilation.

Small changes in ventilation can have a profound effect on pH.

Ventilation is controlled by pH of CSF.

REGULATION OF HYDROGEN ION CONCENTRATION- RESNAL COMPENSATION

PCT Reabsorption of bicarbonate .

CA- regulated.

DCT Addition of new bicarbonate

Excretion of H+

Aldosterone- regulated

Acid base disturbancesThe normal acid-base status

An acid–base disturbance disrupts at least two of these three variables.

pH 7.35-7.45

Bicarbonate (HCO3-)

22-26 mmol/L

PCO2 35-34 mmHg

Base excess-deficitThe base excess-deficit is the amount or base that must be added to blood or removed from it to return pH to 7.4 and to return the paCo2 to 40 mmHg at full oxygen saturation and 37o C.

Positive values indicate metabolic alkalosis.

Negative values indicate metabolic acidosis.

Anion gap It is the difference between major measured cations and

major measured anions.

Anion gap = [Na+] – ([Cl-] + [ HCO3-])

Normal range 12±3 mEq/L (plasma proteins represent 11mEq/L).

Unmeasured cations include K+, Ca++, & Mg++.

Unmeasured anions include PP, phosphates, sulphates and organic acids.

Increased AG in metabolic acidosis reflects an increase in the organic acids.

The delta ratioIncrease in Anion Gap / Decrease in bicarbonate< 0.4 Hyperchloraemic normal anion gap acidosis

0.4 - 0.8

Consider combined high AG & normal AG acidosis BUT note that the ratio is often <1 in acidosis associated with renal failure

1 to 2

Usual for uncomplicated high-AG acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due

to urine ketone loss (esp if patient not dehydrated)

> 2 Suggests a pre-existing elevated HCO3 level so

consider: a concurrent metabolic alkalosis, or a pre-existing compensated respiratory acidosis

Acids are corrosives to their containers!

Respiratory acidosis The respiratory system is unable to remove sufficient CO2 from the body →high PCO2 levels (hypercapnia).

The following reaction becomes displaced to the right by the increased PCO2:

CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

The consequence of this defect is an increased [H+] (i.e. acidosis – reduced pH), and an increased [HCO−

3].

Respiratory acidosis- causes Alveolar hypoventilation

CNS depression Head trauma- drugs NMT Residual NMB Muscles Myopathy- MG Chest wall Flail chest- Kyphoscoliosis Pleura Effusion – pneumothorax Airway obstruction

Upper Laryngeal spasm Lower Severe

bronchospasm Parenchymal lung disease

Pneumonia- ARDS- aspiration pneumonitis- interstitial lung disease ……

CO2 overproduction

MH- thyroid storm- prolonged seizure- CHO overload in TPN

Respiratory acidosis –adverse effects

1 CNS depression up to coma 2 Direct myocardial depression 3 Possible hyperkalemia (transcellular) 4 Respiratory High CO2

Vasculature Systemic VD Hypotension-bounding pulse

Cerebral VD ↑ ICP Pulmonary VC PHT

CNS Depression Narcosis Autonomic Sympasthetic

stimulation Apprehension Sweating Tachycardia

Respiratory acidosis-treatment 1 Measures to ↑

alveolar ventilation

ETT & Mechanical ventilation Bronchodilators. Brain stem stimulants (dopram). Reversal of narcotics (naloxone). Reversal of NDMB.

2 Measures to ↓ CO2 production when↑

Dantrolene- NMB- antithyroid drugs- ↓ CHO intake.

N.B. Sodium bicarbonate

Is rarely needed unless severe acidosis and associated with CVS collapse. Transient ↑ in PCO2 (carbicarb, tromethamine: THAM).

Patients with base line chronic respiratory acidosis require attention.

When they develop acute respiratory failure the aim of therapy is to return PCO2 to their base line as normalizing PCO2 to 40 → metabolic alkalosis Oxygen therapy must be carefully titrated (hypoxic respiratory drive, normalizing PO2 can→ severe hypoventilation).

Respiratory alkalosis Inappropriate alveolar ventilation relative to CO2 production

The following reaction becomes displaced to the left by the decreased PCO2:

CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

The consequence of this defect is a decreased [H+] (i.e. alkalosis – high pH), and a decreased [HCO−

3].

Kidneys will excrete increased amounts of HCO3The renal response has a slow onset and the maximal

response takes 2 to 3 days .

Respiratory alkalosis-causes

1 Hypoxia

Pulmonary Embolism Pneumonia Asthma Pulmonary edema (all types) ↓ Pulmonary compliance.

↑ altitude

2 Neurologic Stroke encephalitis IC tumors 3 Psychiatric Hysterical pain anxiety 4 Sepsis and fever Gram negative septicemia 5 Pregnancy 50%↑ MV- PCO2 around 30mmHg-

bicarbonate↓ -pH 7.44 6 Liver disease A respiratory alkalosis is the commonest acid-

base disorder found in patients with chronic liver disease

7 Intoxication Salicylates toxicity 8 Iatrogenic Ventilator induced (common)

Respiratory alkalosis- adverse effects 1 Hb

ODC →Lt

2 Electrolytes K↓ ECG changes-arrhythmias Ileus weakness

Ca↓ (ionized) NM irritability CVS depression

3 Myocardium Contractile element

↓ Contractility

4 Respiratory ↓ CO2

Vasculature Cerebral Ischemia Systemic SVR↑ Coronary Spasm Placenta Perfusion ↓ Pulmonary PVR↓

Respiratory alkalosis-treatment

1 Correction of the cause

The number one priority is correction of any co-existing hypoxemia

Administration of oxygen in sufficient concentrations and sufficient amounts is essential.

2

Anxiolytics (lorazepam-midazolam)

3 CO2-enriched air (bag and mask rebreathing of CO2) is not recommended

Metabolic acidosisLow pH + Decrease in plasma bicarbonate.Compensation:

Respiratory The low pH will stimulate the chemoreceptors→ hyperventilation (Kaussmaul’s respiration) CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

The respiratory compensation for MA →Lowering PCO2→ moving the equation to the left and thus further ↓ HCO−3

Renal -↑ H+ excretion -↑ reabsorption of all filtered HCO−3

- Generation of new HCO−3

Metabolic acidosis-causes 1 Strong acid

gain →consumption of HCO−3 (High anion gap MA)

Ketoacidosis DM Starvation Alcoholism High fat diet

Lactic acidosis Shock Hypoxia Liver failure (N liver: lactate→ G)

Renal failure Kidney failure to excrete H+

Intoxication Salicylates Methanol Propylene glycol (organic solvent) Cyanide Paraldehyde

2 HCO−3 loss Normal anion gap MA (hyperchloraemic)

GIT Severe diarrhea/fistulae: (pancreatic, biliary, intestinal, ileostomy, uretro-segmoidostomy) /ingestion of large amount of anion exchange resins

Renal PCT RTA-CA inhibitors DCT Hypoaldosteronism- spironolactone

Iatrogenic Rapid ECF expansion with bicarbonate free fluid e.g. Nacl TPN (Cl) Mineral acid administration

Metabolic acidosis-adverse effects

Nausea and vomiting

Abdominal pain

Change in sensorium

Tachypnea

Decreased muscle strength

Decreased myocardial contractility

Arteriolar dilatation

Venoconstriction

PHT

Metabolic acidosis-treatment1

Emergency management of life-threatening conditions always has the highest priority.

E.g. endotracheal intubation, mechanical ventilation, CPR and treatment of hyperkalemia.

Maintain hyperventilation in ventilated patients Expected PCO2= (1.5 x actual bicarbonate) + 8 mmHg.

2 Specific

DKA Insulin, IV fluids, K LA (shocked) Oxygen, fluids, blood, vasopressors and inotropes Salicylates Alkalinization of urine by sodium bicarbonate.

3 Correction of any respiratory component of acidemia

Reversal of NMB. Reversal of narcosis Bronchodilators

4 Losses Fluids Replace deficit Electrolytes Replace deficit Sodium bicarbonate NOT be given on a routine basis

Indications if PH < 7.2 Severe hypobicarbonatemia (<4 mEq/L) Severe hyperchloremic acidemia

Dosage Empirical: 1 mEq/kg

Calculated upon base deficit: BDX BW X 30% In practice half the dose is given.

5 Refractory MA Hemodialysis

Metabolic alkalosis A metabolic alkalosis is a primary acid-base

disorder which causes the plasma bicarbonate to rise to a level higher than expected.

Compensatory hypoventilation Expected pCO2 = 0.7 [HCO3] + 20 mmHg

Hypoventilation may be absent:•Pain •Pain with arterial puncture• Hypoxemia

Metabolic alkalosis-causes

90%

Chloride- sensitive Urine Cl is low<10 mmol/L

Conditions causing ECF volume depletion.

Vomiting CHPS NG suction Diarrhea Diuretics

10%

Chloride- resistant Urine Cl is low>20 mmol/L

Increased H excretion in exchange of Na

↑ Mineralocorticoid activity, Hypoaldosteronism, Caushing Severe hypokalemia

Rare causes Others Addition of base to ECF

Large doses of NaHCO3(+renal insufficiency) Massive blood transfusion (citrate in liver→ bicarbonate) Large doses of sodium penicellin Milk alkali syndrome Re-feeding Recovery from metabolic acidosis

Metabolic alkalosis-adverse effects1 Hb

ODC →Lt

2 Electrolytes K↓ ECG changes-arrhythmias Ileus weakness

Ca↓ (ionized) NM irritability CVS depression

3 Myocardium Contractile element

↓ Contractility

4 Respiratory ↓ CO2

Vasculature Cerebral Ischemia Systemic SVR↑ Coronary Spasm Placenta Perfusion ↓ Pulmonary PVR↓

Metabolic alkalosis-treatment

The cause Cl- sensitive

Nacl infusion (correction of ECF& Na depletion)

Cl- resistant

Aldosterone antagonists(spironolactone) K infusion (correction of K depletion)

Temporary ph>7.6 → vit C, Hcl, NH4cl Acetazolamide to ↑ renal bicarbonate excretion

Refractory Hemodialysis

Metabolic alkalosis-the neglected part of treatment

Hypoxemia is areal danger  1. Hypoventilation (respiratory response to metabolic alkalosis)2. Pulmonary microatelectasis (consequent to hypoventilation)3. Increased ventilation-perfusion mismatch (as alkalosis inhibits

HPVC) 4. Oxygen unloading may be impaired (shift of the ODC to the left). 

The body’s major compensatory response to impaired tissue oxygen delivery is to increase COP but this ability is impaired if hypovolemia and decreased myocardial contractility are present.

 

Give oxygen!

Acid-base approach Step 1. Look at the pH

<7.35—acidosis

7.35-7.45—normal or compensated acidosis

>7.45—alkalosis

Step 2. Look for respiratory component (volatile acid= CO2)

PCO2 <35 mm Hg—respiratory alkalosis or compensation for metabolic acidosis (if so, BD* > −5)

PCO2 35-45 mm Hg—normal range

PCO2 >45 mm Hg—respiratory acidosis (acute if pH <7.35, chronic if pH in normal range and BE > +5)

Step 3. Look for a metabolic component (buffer base)

BD >−5 metabolic acidosis

BE −5 to +5 normal range

BE >5 alkalosis

Acid-base approach

Put this information together:

1 Acidosis CO2 <35 mm Hg ± BD >−5 acute metabolic acidosis 2 Normal range pH CO2 <35 BD >−5 acute metabolic acidosis

plus compensation 3 Acidosis PCO2 >45 mm Hg normal range BE acute respiratory acidosis 4 Normal range pH PCO2 >45 mm Hg BE >+5 prolonged respiratory

acidosis 5 Alkalosis PCO2 >45 mm Hg BE >+5 metabolic alkalosis

6 Alkalosis PCO2 <35 mm Hg BDE normal range acute respiratory alkalosis 7 If acid-base picture doesn’t conform to any of these, a mixed picture is present.