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