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Mazen Kherallah, MD, FCCP, FCCM, FACP Michigan State University Society of Critical Care Medicine
Definition Elevated HCO3 Decline in [H+] in the ECF
Causes of Metabolic Alkalosis
Causes associated with contracted ECF volume Low urine Cl:
± Loss of gastric secretions: vomiting, nasogastric suction ± Remote use of diuretics ± Delivery of nonreabsorbable anion plus Na: Carbenicilline ± Posthypercapnia ± Loss NaCl in GI: congenital Cl loss, villous adenoma
Persistent high urine Cl:
± Bartter¶s-like syndromes ± Current diuretic use
Causes of Metabolic Alkalosis
Causes associated with normal or expanded ECF volume
Large reduction in GFR plus a source of HCO3:
± Alkali ingestion
Enhanced mineralocorticoid activity:
± primary aldosteronism ± Secondary hyperaldosteronism: renal artery stenosis, malignant hypertension, renin producing tumor, low effective arterial blood volume with an alkali load ± Endogenous or exogenous mineralocorticoid, licorice ingestion, ACTH secretion
Metabolic Alkalosis Extracellular elevation of HCO3± Absolute: by addition of HCO3.to the ECF ± Relative: by the loss of ECF volume Intracellular events: ± Hypokalemia: Kaliuresis ± Intracellular acidosis: replacement of K by H .
to a compartment: ± Loss of an anion such as Cl± Retention of a cation such as Na+ - .Addition of HCO3 to the ECF With the constraints of electroneutrality. there are only two ways to add a specific anion HCO3.
in Plasma - Vomiting or nasogastric suction Cl.Anion Gain of HCO3.Addition of HCO3 to the ECF Loss of Cl.loss in urine .
its volume is expanded If GFR is normal this extra Na and bicarbonate will be excreted via the kidney GFR should be low (permission of the kidneys) to retain extra Na and HCO3 .Addition of HCO3 to the ECF Retention of NaHCO3 Gain of HCO3.in Plasma - When Na is retained in the ECF.
Mechanisms for Renal Retention of HCO3 .
are distributed in smaller volume Metabolic alkalosis: contraction alkalosis .Contraction of the ECF Volume Increased [HCO3-] The ECF volume is contracted secondary to removal of NaCl and water The [HCO3-] is increased and the content is unchanged Same HCO3.
thus new HCO3 formation .Contraction of the ECF Volume Diuretic Ingestion Diuretic ingestion causes NaCl loss in the urine and ECF volume contraction Increased production and excretion of NH4 consequent to hypokalemia.
Causes Associated with ECF Volume Contraction .
1. Vomiting or Nasogastric Suction Loss of HCl Generation of HCO3 Excretion of NaHCO3 in the urine ECF contraction Renin will increase angiotensin II and aldosterone Excretion of K: kaliuresis .
5 X 30= 100 mmol intracellular Total HCO3 added is 250 1 liter of gastric fluid contains 100 mmol of H+ and 100 mmol of Cl2.5 liters is needed to be lost before HCO3 is raised to 35 . How many liters of emesis must be lost in order to raise the [HCO3-] in plasma by 10 mmol/L in 70-kg adult? Extracellular [HCO3-] is 25 mmol/L and intracellular is 10 mmol/L 10 X 15= 150 mmol extracellular 3.
Diuretics Diuretics blocks Na and Cl channels More Na is delivered to DCT Na exchange with K under the effect of aldosterone Kaliuresis and hypokalemia ensues Depleted ECF and high aldosterone leads to hypokalemia Hypokalemia augments renal ammoniagenesis .2.
Your computer may not have enough memory to open the image. . and then open the file again.Ammoniagenesis The image cannot be displayed. If the red x still appears. or the image may have been corrupted. Restart your computer. you may have to delete the image and then insert it again.
Your computer may not have enough memory to open the image. Restart your computer. fewer NH4 is reabsorbed because of the competition between NH4 and K. .Ammoniagenesis When K is high in the lumen. you may have to delete the image and then insert it again. With hypokalemia more NH4 is reabsorbed and then secreted as NH3 combining with H and raising the HCO3 in plasma The image cannot be displayed. or the image may have been corrupted. and then open the file again. If the red x still appears.
Intracellular Acidosis in Metabolic Alkalosis associated with Hypokalemia The depletion of K leads to a shift of cation Na and H into the cells This shift exacerbates the degree of HCO3 elevation in the ECF and cause intracellular acidosis Hypokalemia must be corrected first .
In CCD the action of aldosterone will lead to hypokalemia Hypokalemia will cause more ammoniagenesis and thus increased plasma HCO3 and metabolic alkalosis .3. Nonreabsorbable Anions If a patient has a contracted ECF volume and takes an Na salt with an anion that cannot be reabsorbed by the kidney: Carbenicillin There is stimulus for Na reabsorption but it cannot be reabsorbed.
3. Nonreabsorbable Anions Cl in urine should be < 20 Na in the urine should be high Na + K should be > Cl due to the presence of unmeasured anion .
HCO3 is generated in the kidney and excretion of NH4Cl ensues When hypercapnia resolves increased HCO3 content will cause metabolic alkalosis . plasma HCO3 concentration is increased.4. Posthypercapnia During chronic hypoventilation and hypercapnia.
Loss of NaCl via the GI tract Congenital chloridorrhea.5. villous adenoma Loss of Na and Cl in stool Similar to diuretic induced metabolic alkalosis The urine always has Na and Cl .
Bartter-like Syndromes Hypokalemia Renal Na and Cl wasting Contracted ECF volume Metabolic alkalosis hypereninemia Deficiency of Mg Hypertrophy of justaglomerular apparatus High rate of Ca excretion .6.
2 Cl electroneutral cotransporter: NKCC in the Luminal membrane of the thick ascending limb of Henle this causes delivery of Na and Cl to CCD and thus K excretion NaCl wasting and a low ECF volume results in high level of renin . Bartter-like Syndromes The pathophysiology can be considered as having a loop diuretic acting 24 hour a day Defect in Na. K.6.
Causes Associated with Normal or Expanded ECF Volume .
Hyperaldosteronism Aldosterone causes hypokalemia Hypokalemia enhances ammoniagenesis. which enables renal new CO3 formation Hypokalemia causes an increased indirect reabsorption of HCO3 via the rise in proximal tubular intracellular H Hypokalemia reduces GFR and thereby maintains the elevated blood HCO3 .1.
2. Alkali Loading Under usual circumstances. clinically important elevation of plasma HCO3 occur with NaHCO3 administration . NaHCO3 loading leads to only a mild elevation in plasma HCO3 because most of these HCO3 are excreted In the presence of Na depletion or in renal failure.
Magnesium Depletion Mg enhances the NKCC mechanism Depleted Mg results in higher Na and Cl excretion and Hypokalemia with metabolic alkalosis .3.
4. Milk-Alkali Syndrome Ingestion of large amount of milk and absorbable antacids: CaCO3 Patient excrete large amount of Ca and HCO3 in the urine Ca deposits more in alkaline urine Deposition of Ca leads to renal function impairment Thus HCO3 increased in plasma .
Urine Cl . or the image may have been corrupted.The image cannot be displayed. Your computer may not have enough memory to open the image. you may have to delete the image and then insert it again. If the red x still appears. Restart your computer. and then open the file again.
Reabsorption of Na+ in CCD Electroneutral Electrogenic Na Na Na Cl Cl Na Na Na Na-K ATPase K Cl K CCD Cl K K K Cl K .
a 26-year old dancer. She denies vomiting and the intake of medications other than vitamins. Physical examination reveals a thin woman who has a contracted ECF volume.Case # 1 Toby. complains of weakness. .
48 Urine 52 50 0 8 .1 90 32 7.Plasma Na K Cl HCO3 pH 133 3.
Questions???? What acid-base disturbance is present? Why is the Na in urine not lower. given the presence of ECF volume contraction? Why is Toby hypokalemic? What is the basis for the acid-base disturbance? .
Discussion of Case # 1 Metabolic alkalosis with hypokalemia Cl is low in urine because of the ECF volume contraction and reabsorption of NaCl Na is high in the urine because it is excreted with an anion other than Cl The very high urine pH indicated that the other anion is HCO3: bicarbonaturia To the degree that the filtered load of HCO3 exceeds the tubular capacity to reabsorb it. HCO3 are excreted Hypokalemia secondary to high urine delivery to CCD and high aldosterone secondary to contracted ECF volume Body shape disorder and induced vomiting .
Case # 2 Farrah. She jogs 60 Km per week and is asymptomatic. she was surprised to find that she was hypokalemic. she consumes little meat or table salt. When she volunteered for a clinical research project. is concerned about her body image so she diets most of the time. a beautiful person. Her ECF is contracted . Her food intake is erratic and consists mainly of vegetables and fruits. She denied vomiting and the use of diuretics or laxatives.
7 l HCO3 pH Creatinine Osmolality 96 30 7.Plasma a 138 2.7 287 rine 63 34 0 0 5.45 0.6 563 .
Metabolic Alkalosis Is GFR very low Yes No Alkali intake Ion-exchange resins milk alkali syndrome Vomiting Is ECF volume contracted Urine Cl >20 Yes No <10 Waht is the renin and aldo level Diuretics Bartter Mg depletion Loss of gastric fluid Diuretic Rare causes Both low Low renin Hihg aldo Both high Exogenous mineralcorticoids Cushing's syndrome Primary hyperaldosteronism RAS Renin tumor Malignant hypertension .
metabolic alkalosis with hypokalemia and high aldosterone level ECF volume contraction with 0 Cl in urine but high Na Positive urine net charge indicative of an anion other than Cl is present Low pH and high osmolal gap indicates that the anion is not HCO3 (bicarbonate is 0) Negative NaCl balance because of poor dietary intake and nonrenal loss. she has an unusual organic anion load from her diet .Discussion of case # 2 ECF volume contraction.
Each time his condition reverts to normal without therapy . He took antacids to relieve his abdominal pain. but their beneficial effect was transitory.Case # 3 Solly has episodes of abdominal pain and profuse diarrhea for months. More recently he has vomited on occasion and has suffered from episodic tingling and weakness.
50 48 48 4.Plasma pH PaCO2 HCO3 K Anion gap Creatinine Urine volume Admission Not done Not done 62 3.1 15 2.0 13 60 ml .3 4 hours later 7.
Discussion of Case # 3 Metabolic alkalosis with hypokalemia Bicarbonate gain of non-renal cause secondary to gastric HCl secretion Most-likely HCl loss from GI Low rate of excretion of HCO3 due to decreased GFR ECF volume is not contracted due to Low GFR HCl reabsorption led to improvement in metabolic alkalosis Zollinger-Ellison syndrome .
He had a markedly contracted ECF volume. Green is 42 year old and is a chronic alcoholic. he was unkempt and incoherent. He was brought to the emergency room. He had been lying in the park in a pool of vomitus. On physical examination. was febrile (39) and had evidence of pneumonia.Case # 4 Mr. obviously intoxicated. .
9 80 20 1.Plasma a K Cl HCO3 Creatinine rea 130 2.53 25 60 38 150 Weakly Osmolality 320 .4 12 H pH PaCO2 PaO2 lbumin lucose Ketones 30 7.
8 mmol/L from 40 For every mm Hg in Paco2.5 mmol/L from 25 For every mm Hg increase in Paco2. Paco2 should rise 0.7 mm Hg For every twofold increase in Paco2. the plasma H+ should fall by 0.5 mmol/L from 25 Metabolic alkalosis Acute respiratory acidosis Chronic respiratory acidosis Acute respiratory alkalosis Chronic respiratory alkalosis . the plasma HCO3 should fall by 0.Expected Responses to Primary Acid-Base Disorders: Disorder Metabolic acidosis Response Drop the 7 and the decimal point from the pH For every mmol/L fall in HCO3 from 25. Paco2 drops 1 mm Hg Drop the 7 and the decimal point from the pH For every mmol/L rise in HCO3 from 25. the plasma HCO3 should increase by 2. the plasma HCO3 should increase by 0.3 mmol/L from 25 For every mm Hg fall in Paco2.
Discussion of Case # 4 Metabolic acidosis with increased anion gap most likely alcoholic ketoacidosis. and Llactic acidosis type B secondary to thiamin deficiency Metabolic alkalosis with vomiting and hypokalemia Respiratory alkalosis from pneumonia .
E.5 L per day . she becomes lightheaded when she stands up. she enjoys toast with jam along with her traditional cup of tea. blood pressure 150/90 and orthostatic of 15 mm Hg. She has not been feeling well since she took her medicine. and she is less able to perform at her high intellectual level. her urine volume is 0. she feels weak.Case # 5 Emily is 73 year old. and gave her thiazide diuretic. she drinks a lot of water On P. her physician told her that her blood pressure is elevated 170/95. On her annual checkup.
1 0 405 .Plasma a K Cl HCO3 pH Urea lucose Osmolality 107 1.2 108 220 3 rine 12 7 0 5.9 67 30 7.47 4.
his ECF is not low Hypokalemia did not improve with 200 mmol per day. Urine output 2-5 L per day . He developed a UTI and was treated with gentamicin 80 mg q8h for 2 weeks.Is This Bartter¶s Syndrome 50 year old paraplegic male has a neurogenic bladder as a result of MVA. There was no special findings on physical examination.
40 0.48 0.8 105 26 7.6 91 38 7.2 - .6 10 2.5 3 a K Cl HCO3 pH Creatinine UN g olume 140 3.Plasma (admission) Plasma (day 14) Urine 49 36 82 0 5.7 11 2.2 - 140 1.
Driven by lumen positive charges H2O Na+ Na+ Ca++ Mg++ NKCC Na+ 2Cl.ROM K-1 + K + K K+ Na+ K + ATP ClCa receptors also binds cations like gentamicin 2 Na+ 2 ClH2O .
Case # 7 Alicia is a 47 year old with history of Hypertension which is controlled with diuretics. Presented with dizziness and contracted ECF .
46 1.7 99 28 7.0 1 287 Urine 36 61 57 0 5.9 4 563 .Plasma Na K Cl HCO3 pH g Creatinine Osmolality 138 2.
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