ACID –BASE DISTURBANCES

ACID –BASEDISTURBANCES

University of Medicine and Pharmacy, IasiSchool of MedicineANESTHESIA and INTENSIVE CAREConf. Dr. Ioana Grigoras

MEDICINE4th year

English ProgramSuport de curs

WATER AND ELECTROLYTES DISTURBANCES

Classification (Shires şi Baxter)

• Volume disturbances• Volume contraction• Volume expansion

• Concentration disturbances• Hyponatremia• Hypernatremia• Other hyperosmolar states

• Composition disturbances• Hypo/hyperpotasemia• Hypo/hypercalcemia• Hypo/hypermagnesemia• Hypo/hyperphosphatemia• Hydrogen ion disturbances (acid-base disturbances)

• acidemia – H+ concentration >44nmol/l (pH < 7.36)• alcalemia - H+ concentration <36nmol/l (pH > 7.44)• acidosis – the pathological condition which results in

acidemia or would result in acidemia in the absence of compensation;

• alkalosis - the pathological condition which results in alcalemia or would result in alcalemia in the absence of compensation;

Acidosis and alkalosis may coexist and the resultant pH reflects this coexistance. But acidemia and alcalemia are mutuali exclusive conditions.

• Respiratory acidosis – the primary (non-compensatory) elevation of PaCO2

• All the other conditions which result in acidosis are termed as metabolic ones (non-respiratory).

• Respiratory alkalosis – the primary (non-compensatory) decrease of PaCO2

• All the other conditions which result in alkalosis are termed as metabolic ones (non-respiratory).

RESPIRATORY ACIDOSIS

RESPIRATORY ACIDOSIS

• The primary disturbance:

↑ PaCO2 > 45mmHg (hypercapnia)

• Compensatory disturbance change:

↑ HCO3 > 27mmol/l

acute respiratory acidosis

forms

chronic respiratory acidosis

forms

CAUSES • all conditions resulting in type II respiratory failure

RESPIRATORY ACIDOSIS

Mechanisms:•alveolar hypoventilation•severe ventilation/perfusion mismatch

Pathophysiology– ↑ PaCO2

– ↑ CO2 + H2O ↔ H2CO3 ↔ ↑ H+ + HCO3-

acidemia

– Compensation intra/extracellular buffer systems renal

↑ renal bicarbonate reabsorbtion ↑urinnary H+ elimination ↑ urinnary Cl- elimination → ↓Cl-mia

– Anticipated HCO3- level (anticipated compensation)

• Acute respiratory acidosis: for every ↑ PaCO2 of 10mmHg → HCO3↑ with 1 mmol/l

• Chronic respiratory acidosis: for every ↑ PaCO2 of 10mmHg → HCO3↑ with 4 mmol/l

RESPIRATORY ACIDOSIS

CLINICAL PICTURE• Respiratory system:

– respiratory depression ( breathing frequency/amplitude)– rapid shallow breathing– abnormal respiratory pattern

• CNS:– headach, visual disturbances– anxiety, drowsiness– sleepyness, coma– cerebral vasodilation → ICHT

• Cardio-vascular system:– Vasodilation (congestive facies, eye congestion, papillary edema)– sympathetic nervous system stimulation– tachycardia, sweating, HTA– negativ inotropic effect– hTA, rhythm disturbances

RESPIRATORY ACIDOSIS

TREATMENT• Treatmentul of alveolar hypoventilation (hypercapnia)

– Treat causal disease– Respiratory centre stimulation– Ventilatory support (mechanical ventilation)

• Treatmentul of hypoxemia– ↑ FiO2 (masks or cannulae)– Ventilatory support (mechanical ventilation)

• Treatmentul of acidosis– correct settings of artificial ventilation – Acute respiratory acidosis → hyperventilation– Chronic respiratory acidosis:

risk of post-hypercapnic metabolic alkalosis

RESPIRATORY ACIDOSIS

RESPIRATORY ALKALOSIS

RESPIRATORY ALKALOSIS

• Primary disturbance:

↓ PaCO2 < 35mmHg (hypocapnia)

• Compensatory change:

↓ HCO3 < 24mmol/l

CAUSES• Hypoxemia

– Pulmonary diseases: ARDS, pneumonia, pulmonary edema, pulmonary embolism, pulmonary fibrosis

FiO2 – high altitude, closed spaces– Congenital cardiac diseases– Anemia, blood hypotension

• Stimulation of respiratory center– psychogenic hyperventilation (fear, effort)– CNS diseases: trauma, tumors, ICHT, brain stem diseases– Pulmonary deseases: pneumonia, asthma, pulmonary embolism

• Other causes– salicilate intoxication– SIRS, sepsis– liver failure– pregnancy– Hyperventilation during mechanical ventilation

RESPIRATORY ALKALOSIS

Pathophysiology PaCO2

• Compensatory mechanism → HCO3

– Buffer systems– Renal mechanism: → renal HCO3 reabsorbtion

→ ↑ renal HCO3 formationalkaline urine

– Intracellular compartment H+ goes out K+ goes inhypopotasemia

– ↑ bonding of ionized Ca to albumine → plasma ionized Ca → hypocalcemia– Anticipated HCO3

- level (anticipated compensation) • Acute respiratory alkalosis:

for every ↓ PaCO2 of 10mmHg → HCO3↓ with 2 mmol/l• Chronic respiratory alkalosis:

for every ↓PaCO2 of 10mmHg → HCO3↓ with 5 mmol/l

RESPIRATORY ALKALOSIS

CLINICAL PICTURE• Respiratory system:

– Hyperventilation (↑ breathing frequency/amplitude)• CNS:

– Cerebral vasoconstriction– Dizziness, confusion– Loss of conscienceness

• Neuro-muscullar system: ionized Ca → hyperexcitability– parestesias of the lips, tongue and extremities– muscle twiching– Chvostek sign, Trousseau sign– laryngeal spasm, rhythm disturbances– convulsions

RESPIRATORY ALKALOSIS

TREATMENT• Treat the causative condition

• Rebreathing masks – psychogenic hyperventilation

(rebreathing normalizes CO2 )

• correct setting of ventilatory parameters during artificial ventilation

RESPIRATORY ALKALOSIS

METABOLIC ACIDOSIS

METABOLIC ACIDOSIS

= increased H+ concentration due to acids acumulation or alkali loss (base deficit BE > -2mEq/l)

• Primary disturbance:

↓ HCO3 < 24mmol/l• Compensatory change:

↓ PaCO2< 35mmHg

Sum of cations = sum of anions

Na + K + unmeasured cations = Cl +HCO3 + unmeasured anionsNa + ....... = Cl +HCO3 + unmeasured anions

Anion gap = Unmeasured anions

Anion gap = Na – (Cl + HCO3 )

Normal value = 3-11mEq/l

METABOLIC ACIDOSIS

CLASSIFICATION• With increased anion gap

(acids acumulation)

• With normal anion gap (alkali loss)

METABOLIC ACIDOSIS

Metabolic acidosis with increased anion gap

CAUSES– Lactic acid accumulation

• Type A: all shock classes, cardio-respiratory arrest. hypoxia, effort

• Type B: liver failure, leukemia, ereditary lactic acidosis, drugs, toxins (biguanide, alcohool)

– Keto-acids acumulation• Diabetus melitus, starvation, alcohool ingestion

– Phosphate and sulphate acumulation• renal failure

– Acumulation of other substances (intoxications)• Metanol, salicilaţes, etilenglicol

METABOLIC ACIDOSIS

Metabolic acidosis with normal anion gapCAUSES• With hypopotasemia

– Digestive HCO3 loss– diarheea– pancreatic/billiary fistulas/drainage– uretero-sigmoidostomy

– Renal HCO3 loss – Renal tubullar acidosis type 1 and type 2– acetazolamid

• With normo/hyperpotasemia– Acidifying agents - HCl, parenteral feeding– Hypoaldosteronism– Renal tubullar acidosis type 4

METABOLIC ACIDOSIS

Pathophysiology

Metabolic acidosis with increased anion gap • Acids acumulation → H+ excess

• H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O

HCO3- consumption → HCO3

-

• Acidemia → stimulation of respiratory center →

↑ CO2 elimination → PaCO2

METABOLIC ACIDOSIS

Pathophysiology

Metabolic acidosis with normal anion gap• Digestive/urinnary alkaki loss

H+ excess HCO3

- → ↑ Cl-

(hyperchloremic metabolic acidosis)

METABOLIC ACIDOSIS

Pathophysiology• Compensation:

PCO2 = (1,5 x HCO3) + 8

PCO2 = the last two digits of pH

• Acidosis → excess of extracelular H+

intracellular compartment H+ goes in

K+ goes out

hyperpotasemia

METABOLIC ACIDOSIS

CLINICAL PICTUREAcidosis → generalized celullare dysfunction

• Respiratory system:– Küssmaul breathing

• CNS:– Sleepiness, coma

• Cardio-vascular system:– Vasodilation– Stimulation of SNS– Negative inotropic effect– rhythm disturbances

• Digestiv system:– Nausea, vomiting, diarheea

• Physiological effects:– Hi\yperpotasemia– Right shift of hemoglobin dissociation curve– ↑ ionized Ca

METABOLIC ACIDOSIS

PRINCIPLES of TREATMENT• Treatment of the causative disease

• Treatment of acidemia– Sodium bicarbonate is indicated when pH <7,15-7,10

– Goal of bicarbonate administration is pH ~ 7,20 ( NOT normal pH)

– Estimation of needed bicarbonate amount:

mEq = 0,5 x kg x (14 – HCO3)

mEq = 0,5 x kg x (10 – BE)

– Side effects of bicarbonate administration: sodium overload, hyperosmilarity, metabolic alkalosis by over-compensation, paradoxic intracellular acidosis, hypopotasemia

• Monitoring of treatment: pH, K

• During correction of acidosis K administration may be needed (when the patient has potasium depletion)

METABOLIC ACIDOSIS

METABOLIC ALKALOSIS

METABOLIC ALKALOSIS

= base accumulation

(base exces BE > + 2,5 mEq/l)

• Primary disturbance

primary increase of HCO3 > 27mmol/l

• Compensatory change

secondary increase of PaCO2> 45mmHg

CAUSES• Excessive alkali intake/administration

– Milk-alkali syndrome– Massive blood transfusion– Bicarbonate administration (overcompensation of metabolic acidosis)

• Volume and chloride depletion– Gastric losses (vomiting, fistula, piloric stenosis, …)– Renal losses (diuretics, Bartter sdr, posthypercapnic metabolic alkalosis)

• Mineralo-corticoids excess– Primary hyperaldosteronism– Cushing syndrome– Corticoids administration

METABOLIC ALKALOSIS

CLASIFICATION• Chloride-responsive metabolic alkalosis

Urinary Cl < 10mEq/lGastric losses or diarrheeaDiuretics

• Chloride-unresponsive metabolic alkalosisUrinary Cl > 20mEq/lPrimary hyperaldosteronismCorticoids administrationExcessive alkali intake/administration

METABOLIC ALKALOSIS

PATHOPHYSIOLOGY• ↑ HCO3

- + H+ ↔ H2CO3 ↔ ↑ CO2 + H2O (minutes)

↑ PaCO2

external ventilation → ↑ PaCO2

(hours) limited by PaO2 regulation

limited compensation

• Intracellular compartment H+ out K+ in

hypopotasemia• ↑ albumin-bound ionized Ca → plasma ionized Ca → hypocalcemia

METABOLIC ALKALOSIS

PATHOPHYSIOLOGY

the most frequent acid-base disturbanceHypochloremic contraction metabolic alkalosis

Hypovolemia → RAA system→ ↑ Na, water and bicarbonate reabsorption

Compensation:PaCO2= (0,7 x HCO3) + 21

METABOLIC ALKALOSIS

CLINICAL PICTURE• Respiratory system

• Alveolar hypoventilation• Hypoxemia

• Cardio-vascular system• Hypovolemia/blood hypertension• Arhythmia

• CNS• Lethargy, coma• Convulsions

• Metabolic• Hypopotasemia• Hypocalcemia

METABOLIC ALKALOSIS

DIAGNOSIS– Intravascular volume evaluation

– Presence/absence of blood hypertension

– Plasma K evaluation

– Urinary Cl evaluation

METABOLIC ALKALOSIS

TREATMENTmild/moderate form (BE <12, HCO3 <40)

• Contraction alkalosis– Volume repletion with chloride rich isotonic /colloid solutions– Potasium administration (20mEq / 500ml)– Causative treatment

• Mineralo-corticoid excess– Causative treatment– Spironolactone for correction of potasemia

• Exogenous alkali excess– Stop the administration

severe form (BE >12, HCO3 >40)– Acidifying treatment to alleviate alkalosis– HCl – for immediate pH neutralization; 0,1N solution (100mEq/l)– Amoniu chloride – metabolized to release H+; 2,4% solution (400mEq/l)– Start with 50% of BE; pH monitoring

METABOLIC ALKALOSIS