Clinica Medica & Nefrologia Universita’ degli Studi di ParmaClinica Medica & Nefrologia...
Transcript of Clinica Medica & Nefrologia Universita’ degli Studi di ParmaClinica Medica & Nefrologia...
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Metabolic alkalosis
Enrico Fiaccadori
Clinica Medica & Nefrologia Universita’ degli Studi di Parma
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Metabolic alkalosisMetabolic alkalosis
• An acid-base disorders characterized by increased serum bicarbonate levels (> 26 mEq/L)
• pH values can be increased (alkalosis withpH values can be increased (alkalosis with alkalemia)
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Negative effects of metabolic alkalosisNegative effects of metabolic alkalosis
left shift hemoglobin dissociation curvee s e og ob d ssoc a o cu e reduced cardiac stroke volume reduced cerebral perfusion reduced cerebral perfusion cardiac arrhythmias d d i t d i reduced respiratory drive
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HCO3 58 mmol/L, pH 7,56, PCO2 65, 2K 1.8 mol/L
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Post-hypercapnic alkalosis and respiratory complications in the ICU
% of patients
60
70
• Metabolic alkalosis50
60 • Metabolic alkalosis also associated with longer ICU stay (14.7 vs 9 5 days)
30
40
metab alk
vs 9.5 days)
20
30norm
0
10
Banga A et al COPD 2009; 6:437 440ventilatordependance
Banga A et al., COPD 2009; 6:437-440
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The adaptation to metabolic alkalosis (“compensation”) is by the respiratory( compensation ) is by the respiratory
system (ventilatory depression)
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Henderson-Hasselbalch Equation
(Renal-Metabolic)Metabolic Alkalosis
H 6 1 l HCO3
(Renal Metabolic)
pH = 6.1 + log CO3
H COH CO pC
H2CO3(Pulmonary)Respiratory CompensationH2CO3 pC
CO
p
pCO2
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Respiratory adaptation to metabolic alkalosis
pH = 6.1 + log pCO2
HCO3p g pCO2
6060m
mH
g
4045505560
4045505560pC
O2
m
2025303540
2025303540
0.7 mmHg/mEq HCO3
101520
101520
2 5 10 15 20 25 30 35 40 45 502 5 10 15 20 25 30 35 40 45 50
[HCO3] mEq/l
pCO2 should increase > 45 mmHg and usually is <55pCO2 should increase 45 mmHg and usually is 55
~~~~
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M t b li lk l iMetabolic alkalosisThree pathogenetic aspectsThree pathogenetic aspects
1. Generation
2 Maintenance2. Maintenance
3. Recovery
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M t b li lk l i1 Generation: by addition (direct or indirect) of alkali to
Metabolic alkalosis1. Generation: by addition (direct or indirect) of alkali to
body fluids: ingestion of new alkali (bicarbonate, citrate etc.) or extrarenal production of new alkali ) p(nasogastric suction, vomiting etc.)
2. Maintenance: by changes in renal function that prevent the normally rapid excretion of the excess alkali:alkali: a) Renal failure; b) Tubule ion transport is altered in a way that limits ) p yor prevents bicarbonate excretion, or that increases new bicarbonate production in the distal nephron
3. Recovery
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Vomiting/NG Suctiong
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Proximal Tubule HCO3 ReabsorptionThe Apparent TmaxThe Apparent Tmax
35
40
n
Volume K+
pCO2
25
30
35
orpt
ion
FR
NormalVolumeK+
pCO2 PTH
15
20
25
Rea
bso
Eq/l
GF K
pCO2PTH
5
10
15
HC
O3
Rm
E
A bicarbonate load is rapidly excreted because usually is
associated with volume expansion
0
5
0 5 10 15 20 25 30 35 40
H associated with volume expansion
Plasma HCO3 mEq/l
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Maintenance of metabolic alkalosis: theMaintenance of metabolic alkalosis: thekey is the kidney
The pathophysiologic question: Why is bicarbonatehandling in the kidney maladaptive in metabolic alkalosis?
The pathophysiological answer: not only the excessThe pathophysiological answer: not only the excessbicarbonate is not excreted, but bicarbonate is increasinglyproduced by the kidney
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Three parts of the answer:
- Bicarbonate reabsorption is increased in the proximaltubule (all the filtered bicarbonate is reclamed)
- Bicarbonate is not secreted in the distal nephron asshould be
- Bicarbonate generation is increased in the corticalcollecting duct (new bicarbonate ions are produced by H+g ( p ysecretion)
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Renal bicarbonate handling g10%
ReabsorbedFiltered HCOFiltered HCO3~4,000 mEq/d
90% Reabsorbed
Generation1 mEq/Kg/day
Reabsorbed
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Proximal reabsorption of HCO3-
(R l i i f filt d bi b t )(Reclaiming of filtered bicarbonate)
LUMEN INTERSTITIUMNa+ 3Na +
2K +NHE-3Na+/K+/2Cl-
H+HCO3- HCO3
-H+ Na+
NHE-3
H2CO3-
H2CO3-
CA II3HCO3
-
NBE
CO2 CO2 H2O
CA IV
H2O AQP1 Stimulated by:- Filtered load of HCO3
-
- Luminal H+
- Intracellular acidosis (K depl)- Sodium avidity (ANG II)**ANG II PKC
phosphoryl and activ NHE-3
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Bicarbonate secretionin the distal nephron
A intercalated cells: proton secreting cells
B intercalated cells: bicarbonate secreting cells
Bicarbonate secretion through pendrin is stimulated by alkalosis
Bicarbonate secretion is made possible only if Cl is present in the lumen)only if Cl is present in the lumen)
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The Pendred syndrome: an autosomal recessive disorderThe Pendred syndrome: an autosomal recessive disorder linked to mutations on chromosome 7
The affected gene directed the synthesis of the SLC26A4The affected gene directed the synthesis of the SLC26A4 transporter, later named Pendrin
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Bicarbonate regeneration by H+ secretion in CCT
Stimulated by:- Intracellular
id i (K d l)acidosis (K depl)- Sodium avidity (aldo)
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K+ and H+ secretion in cortical collecting duct are dependent from Na reabsorption by ENaCdependent from Na reabsorption by ENaC
1. In the principal cells od corticalcollecting duct Na-K-ATPasegmaintains a low intracellularconcentration of Na1
2 2. Na enter the cell throughENaC, creating a lumen-positive gradient in the lumen
23
Cl-
positive gradient in the lumen(electrogenic transport)
3 K+ and H+ leave the cells to the3. K+ and H+ leave the cells to thelumen utilizing specificchannels, respectivelypotassium channels ROMK orpotassium channels ROMK orthe H+ATPase, along theelectric gradient
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ENaC activity is increased by:ENaC activity is increased by:
• Flow rate (Na+ delivery)• Flow rate (HCO -• Flow rate (HCO3
delivery)Ald t• Aldosterone
• Alkalemia (basolateral or (tubular fluid bicarbonate)
Gennari FJ. Am J Kidney Dis 2011; 58:626-636
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Gennari F J Am J Kidney Dis. 2011 58:626-636.
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Bases for increased serum bicarbonatelevels in metabolic alkalosis
The central role ofrole of
chloride losses
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The effects of Cl and K depletionth i t f t b li lk l ion the maintenance of metabolic alkalosis
Gennari FJ. Am J Kidney Dis 2011; 58:626-636
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Central role of chloride depletion:pCl is more important than K
Same K depletion but different Cl intake:
more severemore severe metabolic alkalosis in
low Cl diet
Gennari F. Am J Kidney Dis 2011 58:626-636
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Central role of chloride depletion:pCl- is more important than volume
expansion
Cl- repletion in the face of persistent
expansion
Cl- repletion in the face of persistent volume depletion corrects metabolic
alkalosis whereas volume expansionalkalosis, whereas volume expansion without Cl- not
Rosen RA et al., Am J Med 1988; 84:449-458
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Wh t i th l f t iWhat is the role of potassium depletion in metabolic alkalosisp
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Cellular cationic shifts in K depletionCellular cationic shifts in K depletion
K +
Na+
H+
I t ll l id i d t K d l tiIntracellular acidosis due to K depletion increases glutamine catabolism increased production of NH increased excretion ofproduction of NH3 increased excretion of NH4
+ increased bicarbonate production
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Am J Kidney Dis. 2011 58:626-636.
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Causes of metabolic alkalosis in theCauses of metabolic alkalosis in thepast were categorized based on the
t t t t ( lresponse to treatment (volumeresponsive/contraction alkalosis etc.)rather than on the specificpathophysiological processpathophysiological process
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Gennari F, J Am J Kidney Dis 2011 58:626-636
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Differential diagnosis
Gennari FJ, J Am J Kidney Dis 2011 58:626-636
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Not always the causes leading to metabolic alkalosis are evident from history physical examination and urine analysisevident from history, physical examination and urine analysis
MetabolicMetabolic alkalosis:
peculiarities for the ER physician
Joo-Hark Yi et al Am J Kidney Dis 2012 in press
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Urine anion gap=
[Na] + [K]- [Cl]
If UAG has a positive value presence of unmeasured anion
(if pH > 7 is bicarbonate)( p )
Joo-Hark Yi et al., Am J Kidney Dis 2012 in press
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Metabolic alkalosis: treatment
LOW URINE CHLORIDE KIDNEY FAILURE True Volume Depletion
NaCl Expansion “Effective” Intravascular Depletion
KIDNEY FAILURE Dialysis HCl
Effective Intravascular Depletion(CHF, Cirrhosis, Nephrotic Syndrome) Acid - HCl, NH4Cl, Arginine Cl Acidifying Diuretics (Acetazolamide 250-500 mg x2-3 p.o) +KCl
Surgical Hyperaldosteronism/Mineralocorticoid Excess States
Acidifying Diuretics (Acetazolamide 250 500 mg x2 3 p.o) KCl
HIGH URINE CHLORIDESurgical Hyperaldosteronism/Mineralocorticoid Excess States Surgery
Non-Surgical Aldosteronism – Spironolactone/Eplerenone Exogenous M.C. – Stop Drugs/Agentsg p g g Genetic Disorders
Bartter/Gitelman –KCl, Mg, NaCl, Spironolactone, Eplerenone,Amiloride, ACEI, PG Inhibitors (primarily for Bartter) Liddle – Amiloride/Triamterene (Not Spironolactone or Eplerenone) Cl diarrhea - Replace K, PPI, Organic Acid Salts
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Joo-Hark Yi et al., Am J Kidney Dis 2012 in press
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Joo-Hark Yi et al., Am J Kidney Dis 2012 in press
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Diagnostic ApproachLow Urine Chloride < 15 mEq/l
Volume Contracted/HypotensiveVolume Contracted/HypotensiveNaCl Responsive
Gastrointestinal Causes•Vomiting• Nasogastrric Suction• Nasogastrric Suction• Chloride-Wasting Diarrhea Low Urine Chloride < 15 mEq/lDiarrhea
(Chloridorrhea)• Villous Adenoma
“Effective” Intravascular
qNaCl Unresponsive
Post-HypercapniaCystic FibrosisDiuretics* (Late)
Effective Intravascular Volume Deficit
(Total ECF Volume often –CHF Ci h i N h ti S )Diuretics (Late) CHF, Cirrhosis, Nephrotic S.)
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Diagnostic ApproachHigh Urine Chloride > 15 mEq/l
NaCl Unresponsive
Volume Contracted/HypotensiveVolume Expanded/Hypertensive
• Diuretics* (Early)• Bartter Syndrome
Git l S d
yp
ADRENAL/HORMONAL DISORDERS
• Hyperaldosteronism • Gitelman Syndrome• Hyperaldosteronism• Cushing Syndrome
• Pituitary or Adrenal• Ectopic ACTHEctopic ACTH
• Exogenous Steroids• Licorice/Carbenoxalone11- Hydroxysteroid Dehydrogenase y y y g
ActivityLiddle SyndromeAlkali Ingestion/Infusion g
with Kidney Fx Milk Alkali Syndrome
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Distal reabsorption of HCO3-
LUME INTERSTITIα-intercalated cellLUMEN
INTERSTITIUM
Cl-
α-intercalated cell (collecting tubule)
H+HCO3-
HCO3-
H+
H2CO3-
H2CO3-H+-ATPase
H2CO3
CO2 CO2 H2O
ATP
H2O Stimulated by:- Filtered load of HCO3
-
- Luminal H+
- Intracellular acidosis (K depl)- Sodium avidity (ANG II)*
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Glutamine transporters and ammoniagenesis pathway in a proximal tubular cellpathway in a proximal tubular cell.
Shiak A. H.Am J Physiol Renal Physiol 301: F969–
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Differential diagnosis
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Pendrin activity in maintenance or recovery of
metabolic lk l ialkalosis