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