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Seminar on acid base disorders nephrolog

Seminar on acid base disorders nephrolog

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Moderator Dr Nebiyu (Internist, Consultant Nephrologist) Presenters Dr Yoseph (R1) Dr Bisrat(R2) July 16,2024 ACID BASE DISORDERS
Outline ●Basic concepts ●Arterial blood gas analysis ●Metabolic acidosis ●Metabolic alkalosis ●Respiratory acidosis ●Respiratory alkalosis ●Case discussion 04/01/2025 2
Basic concepts ● Acid-base disorder; change in normal value of extracellular PH that results when renal or respiratory function is abnormal or when acid or base load over whelms excretory capacity. ● Acidemia-decrease in blood PH below normal range (<7.35) • Acidosis-is process that increases H+ by increasing pco2 or decreasing HCO3 − ● Alkalemia-elevation of blood PH above normal range(>7.45) 04/01/2025 3
4 Hydrogen Ion Concentration and pH 04/01/2025
Cont... ● Respiratory acidosis- A disorder that elevates PaCO2 & reduces PH ● Respiratory alkalosis- A disorder that reduces PaCO2 & elevates PH ● Metabolic acidosis- A disorder that reduces HCO- 3 & PH ● Metabolic alkalosis- A disorder that elevates HCO- 3 & PH ● Simple acid-base disorder- The presence of one of the above disorders with the appropriate respiratory or renal compensation. ● Mixed acid-base disorder- The simultaneous presence of more than one acid-base disorder. 04/01/2025 5
Cont…. 04/01/2025 6
7 Arterial PH is maintained by 3 regulatory mechanisms 04/01/2025
RESPIRATORY REGULATORY MECHANISM ● Regulate PaCo2 in association with CNS (medullary chemo receptors) to defend PH  During metabolic alkalosis→ ↓ventilation(PaCo2 ↑)  During metabolic acidosis→ ↑ventilation(PaCo2↓) 04/01/2025 8
RENAL REGULATORY MECHANISM  3 mechanisms I. Reabsorption of filtered HCO3 - II. Excreation of NH4 in urine III. Formation of titrable acid 04/01/2025 9
ABG ANALYSIS ● ABG is a test that measures PH/PaCO2/PaO2/ SaO2/HCO3 concentration on arterial blood ● Used for:- ○ Identification and monitoring of acid-base disturbances ○ Measurement of PaO2 and PaCO2 ○ Assessment of the response to therapeutic interventions(eg, Insulin in DKA) ○ Detection and quantification of the levels of abnormal hemoglobin ○ Procurement of a blood sample in an acute emergency when venous sampling is not feasible. 04/01/2025 10
Absolute ● An abnormal modified Allen's test ● Local infection or distorted anatomy at the puncture site, ● Severe peripheral vascular disease of the artery selected for sampling ● Active Raynaud's Relative ● Supra therapeutic coagulopathy (INR 3, aptt 100 ≥ ≥ seconds and infusion of thrombolytic agents ● A platelet count <50 x 109 Contraindications for ABG sampling 04/01/2025 11
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ABG Sampling sites 04/01/2025 13
Cont'd 04/01/2025 14
Arterial Vs Venous Gas Analysis VALUES ARTERIAL BLOOD VENOUS BLOOD PH 7.4(7.35-7.45) 7.36(7.31-7.41) PaO2 80-100 mmHg 35-40 mmHg O2 SATURATION 95% 70-75% PaCo2 35-45 41-51 HCO3 22-26 22-26 BASE EXCESS -2 to +2 -2 to +2 04/01/2025 15
Metabolic Acidosis ● Metabolic acidosis is defined as a pathologic process that, when unopposed, increases the concentration of H+ in the body and reduces HCO3. ○ ↓PH,↓HCo3,↓PaCo2 ● Mechanisms ○ ↑ Acid production ○ Loss of bicarbonate ○ ↓ Renal acid excretion ○ Dilutional acidosis 04/01/2025 16
Cont’d ● The serum anion gap can be used to categorize MA into two groups ○ High anion gap MA ○ Normal anion gap MA ● Blood cations(+ve) must be balanced with anions(-ve) to maintain electroneutrality ○ but when comparing main anions(Cl-,HCo3-) with main cations (Na+,K+),there is shortage of anions this is termed ANION GAP, which is 10-14(use 12 as absolute value) 04/01/2025 17
Cont’d ● This gap is due to anions which are difficult to measure(SO4-, pO4-, - vely charged proteins). ○ Anion Gap = Na - (Cl + HCo3) ○ Use 12 as an absolute value for AG ○ ↓1gm/dl albumin = add 2.5mmol to the Anion Gap  Corrected serum anion gap = (Serum anion gap measured) + (2.5 x [4.5 - Observed serum albumin]) ● An increase in the AG is most often due to an increase in unmeasured anions and, less commonly, may be due to a decrease in unmeasured cations (calcium, magnesium, potassium).  a serum potassium of 6 mEq/L will reduce the anion gap by 2 mEq/L 04/01/2025 18
Special Scenarios ● A decrease in the AG can be due to 1. The addition to the blood of abnormal cations, 2. A reduction in the plasma albumin 3. A decrease in the effective anionic charge on albumin by acidosis; 4. Hyperviscosity and severe hyperlipidemia. 04/01/2025 19
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22 Clinical features  Profound effect on nervous, respiratory and cardiac system.  Depressed CNS (lethargy, stupor, coma), headache  Increased ventilation (Kussmaul breathing)  Depressed cardiac contractility but normal inotropic function due to catecholamine release  Peripheral vasodilation, central vasoconstriction  Predisposed to pulmonary edema with minimal fluid due to low pulmonary vasculature compliance  Glucose intolerance 04/01/2025
Respiratory compensation  The development of metabolic acidosis will normally generate a compensatory respiratory response  With normal respiratory compensation, Pco2 decreases by 1.2 mm Hg for every 1 mEq/L net decrease in [HCO3–]. 04/01/2025 23
Cont’d  PCO2 = (1.5 x HCO3 + 8) ± 2.  This equation, which is called Winter’s formula, was derived in children, half of whom were between two months and two years of age.  PCO2 = HCO3 + 15.  The PCO2 should approximate the decimal digits of the arterial pH. 04/01/2025 24
Cont….  These rules work well for mild to moderately severe metabolic acidosis (HCO3 between 7 and 22 mEq/L).  For more severe metabolic acidosis (HCO3 less than 7 mEq/L), the pCO2 should be maximally reduced to the 8 to 12 mmHg range.  As an example: pH = 7.30; pCO2 = 30 mmHg (4.0 kPa); 04/01/2025 25
The delta anion gap/ delta HCO3 ratio in high anion gap MA  When the AG increases in magnitude as a result of metabolic acidosis, that increase should be compared with the magnitude of the fall in HCO3.  This represents the delta AG/delta HCO3 ratio.  Opposite changes in the serum AG and HCO3 concentration would result in a delta AG/delta HCO3 ratio of 1:1 04/01/2025 26
Cont'd  A delta AG/delta HCO3 ratio below 1 suggests one of the following:  A coexisting normal AG metabolic acidosis .  A high AG acidosis in which both renal function is preserved and the acid anion is readily excreted into the urine  Patients with renal tubular acidosis of early renal insufficiency  A delta AG/delta HCO3 ratio of 1:1 is consistent with an 04/01/2025 27
Cont'd  A delta AG/delta HCO3 ratio between 1 and 2 generally occurs with high AG metabolic acidosis, such as lactic acidosis, when renal function is reduced and the acid anions are, thereby, all retained in the body. Metabolic alkalosis coexists with a high AG metabolic acidosis or  When the baseline HCO3 level is elevated as a result of chronic respiratory acidosis. 04/01/2025 28
Cont'd ● Delta AG/delta HCO3 ratio above 2 usually suggests that metabolic alkalosis coexists with a high AG metabolic acidosis or that the baseline HCO3 level is elevated as a result of chronic respiratory acidosis. 04/01/2025 29
Renal vs Extrarenal causes of MA  Renal and extrarenal causes of metabolic acidosis can be distinguished by measuring urinary ammonia excretion.  Because most laboratories do not measure urinary ammonia, one can indirectly assess ammonia excretion by measuring the urinary anion gap (UAG). 04/01/2025 30
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Renal tubular acidosis  In RTA metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.  All forms of RTA are characterized by a normal anion gap (hyperchloremic) metabolic acidosis. 04/01/2025 32
Cont’d 04/01/2025 34
Treatment of MA ● General approach ○ Reverse the underlying pathophysiologic mechanism ○ General vs specific approach ○ Consider acute and chronic forms of MA separately ● Acute MA ○ Alkali therapy ■ Severe acidemia with pH<7.1 ■ pH 7.1-7.2 with severe acute kidney injury (ie, a twofold or greater increase in serum creatinine or oliguria) 04/01/2025 35
Cont… 04/01/2025 36
Chronic MA  The most common causes of chronic metabolic acidosis are diarrhea, advanced chronic kidney disease, and the various forms of RTA  Alkali therapy  Consider benefits of therapy The rational for alkali therapy is summarized here:  Increasing the bicarbonate concentration reduces or eliminates the need for compensatory hyperventilation and can alleviate the dyspnea experienced by some patients.  Chronic metabolic acidosis may have adverse effects on muscle function and metabolism, skeletal integrity, hormone levels, and other physiologic parameters. In children, for example, correction of chronic metabolic acidosis restores skeletal growth 04/01/2025 37
Cont…  Patients with chronic distal (type 1) RTA are likely to develop nephrocalcinosis and calcium-containing kidney stones. This defect can be reversed with adequate bicarbonate replacement.  Chronic metabolic acidosis in patients with kidney dysfunction may accelerate the progression of their kidney damage, and reversal of the acidosis can slow this process 04/01/2025 38
Dosing of alkali therapy (when given) ● Ampules of hypertonic sodium bicarbonate are available as 8.4 percent (50 mEq/50 mL), 7.5 percent (44.6 mEq/50 mL), and 4.2 percent solutions (25 mEq/50 mL).  Acute metabolic acidosis ● The initial goal is a pH >7.2 and/or serum bicarbonate concentration >16 mEq/L. ● Infuse 2 ampules (100 mL) of 7.5 percent sodium bicarbonate (44.6 mEq/50 mL) over 1 to 2 minutes and remeasure the blood pH and serum bicarbonate concentration (eg, after two hours). ● If the distribution space is approximately 55 percent of the body weight (as it is in healthy individuals), the serum bicarbonate level should increase by approximately 2 to 3 mEq/L. 04/01/2025 39
Cont..  Chronic metabolic acidosis – When chronic alkali treatment is required, options include the sodium or potassium salts of either bicarbonate or a metabolizable anion such as citrate or lactate  The potassium salts are indicated when hypokalemia and total body potassium deficits exist. In general, the initial dose is 50 to 100 mEq per day, which is then titrated up, or down, as required.  If ongoing bicarbonate losses persist or accelerate, the dose will need to be adjusted accordingly 04/01/2025 40
Cont’d Treatment goal  Increase [HCO3] to 10-12mmol/L and the PH to 7.20 ● Preferred alkali is NaHCO3 ○ HCO3 deficit= HCO3 space * HCO3 deficit/L ○ HCO3 space= (0.4 + (2.6/HCO3)) * lean body weight 04/01/2025 41
42 Lactic Acidosis  Lactate is an end product in glucose metabolism  Formed by reduction of pyruvate catalyzed by LDH  Principal sites of production are skeletal muscle (25%), skin (25%), red blood cells (20%), brain (20%), and intestine (10%).  Activated neutrophils are an additional source of lactate in inflammatory conditions like ARDS  The concentration of lactate in plasma is usually 2 mmol/L, with a lactate:pyruvate ratio of 10:1  Lactate is cleared from plasma by the liver (60%), kidneys (30%), and heart (10%). 04/01/2025
43 Lactic Acidosis ● The most common cause of metabolic acidosis in hospitalized patients ● Lactate level >2mmol/L –hyperlactatemia ● Lactate level > 4mmol/L – lactic acidosis ● D-Lactic acid acidosis – formed by gut bacteria ● L-lactic acid acidosis ○ Type A ○ Type B 04/01/2025
44 Type A – hypoxic (Poor tissue perfusion) ● Circulatory insufficiency (septic/hypovolemic shock, heart failure, mesenteric ischemia) ● Severe anemia ● Mitochondrial enzyme deficiency ● Inhibitors (carbon monoxide, cyanide) 04/01/2025
45 Type B – non hypoxic (aerobic disorders) ● Severe infections (malaria, cholera) ● Renal failure ● Hepatic failure ● Seizure ● Thiamine deficiency Drugs/toxins ● NRTIs ● Metformin – primarily in renal insufficiency. Treated with dialysis ● Isoniazid ● Fructose ● Acetaminophen depletes glutathione  pyroglutamic acidemia in critical illness ● Ethanol, methanol, propylene glycol 04/01/2025
46 L-Lactic acidosis treatment ● Correct underlying cause. ● Restore tissue perfusion ● Alkali therapy for severe, acute academia ○ Alkali therapy if indicated(Severe acidemia (PH<7.00) to improve cardiovascular function.)  Therapeutic goal ● To raise arterial PH to no more than 7.2 or the [HCO3] to no more than 12meq/L over 30-40mins ○ HCO3 not an effective buffer unless pH is very low ○ NaHCO3 may worsen acidosis by stimulating lactate production (phosphofructokinase) ○ Overshoot alkalosis (lactate is converted to bicarbonate) ○ It is a CO2 burden that must be removed by the lungs. Carbicarb is a commercially available buffer solution that is a 1:1 mixture of sodium bicarbonate and disodium 04/01/2025
Cont’d ● DKA= standard DKA mx ● Alcoholic ketoacidosis ○ Fluid replacement therapy with saline and 5% dw ○ Corection of electrolyte disturbance ● GI bicarbonate loss ○ Treat the cause ○ Volume replacement and alkali therapy when indicated 04/01/2025 47
Reverse/prevents ● Reduced left ventricular contractility ● Arrhythmias ● Arterial vasodilation ● Impaired responsiveness to catecholamine Potential harms of bicarbonate therapy ● Increased arterial and tissue capillary PCO2 ● Acceleration of lactate generation ● Reduced ionized calcium ● Hypernatremia ● Extracellular fluid volume expansion Benefits of HCO3 therapy 04/01/2025 48
Cont’d ● CKD ○ Currently the 2013 Kidney Disease Improving Global Outcomes (KDIGO) guidelines recommended that, in patients with CKD and metabolic acidosis, alkali therapy be used to maintain the [HCO3] in the normal range (23 to 29 meq/L). ○ Renal replacemnt therapy ● RTA ○ Maintenance of normokalemia ○ Alkali therapy with sodium and potassium citrate ○ Mineralocorticoid therapy ○ Diuretic therapy 04/01/2025 49
Classic distal RTA ● Administration of NaHCO3 or sodium citrate with a goal of correcting the HCO3 to normal level. ● Concomitant administration of potassium in acutely acidotic patients with hyopkalemia. ● Alkali therapy decrease frequency of nephrocalcinosis, improve bone density and resume normal growth pattern in children. Generalized distal RTA ● Restore normokalemia. 04/01/2025 50
Metabolic Alkalosis  Metabolic alkalosis is caused by retention of excess alkali and is characterized by ↑PH, HCo3, PaCo2 ↑ ↑  Hypoventilation, producing a secondary increase in arterial Pco2. 04/01/2025 51
● Three factors play key roles: ○ Chloride depletion ○ Abnormal aldosterone secretion, and ○ Hypokalemia. 04/01/2025 52 Cont’d
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Features ● The most important adverse effect is hypokalemia,which increase the likelihood of cardiac arrythmia(esp. in pts with underlying cardiac dysfunction) ● Usually pts with Hco3 level up to 40mmol/l can be assymptomatic but when > 50 mmol/l may develop seizures,tetany,delirium or stupor. 04/01/2025 57
Respiratory compensation ● The PCO2 raises by 0.7mmHg for every 1mEq/L elevation in serum HCO3 concentration ○PCO2=HCO3 + 10 ○PCO2 = 40 + 0.7 × ([HCO3 ] 24) − 04/01/2025 58
Diagnosis ● Diagnosis of metabolic alkalosis involves three steps. ● The first step ○ Detection, is most often based on the finding of elevated venous [total CO2]. ● The second step ○ evaluation of the secondary response (hypoventilation), excluding the possibility that a respiratory acid-base abnormality is also present. ○ This step requires measurement of arterial pH and Pco2. ● The third step ○ Determination of the cause 04/01/2025 59
Cont’d ●Serum [total CO2] levels above 30 mmol/l in association with hypokalemia are virtually pathognomonic of metabolic alkalosis. 04/01/2025 60
Cont’d 04/01/2025 61
Treatment  What is the cause of excessive serum HCO3 concentration?  Why is the excess HCO3 not excreted through the urine? 04/01/2025 62
Treating factors that increase HCO3 production GI H+ loss - PPIs or H2-blockers - Reduce gastric suctioning Intracellular H+ shift - Correction of hypokalemia Exogenous alkali administration - Discontinue all alkali including Na+ and K+ salts of any organic anion that will later be metabolized to HCO3 Excessive Renal H+ loss - Discontinue diuretics. 04/01/2025 63
Treating factors that impair renal excretion of HCO3 1. Reduced arterial blood volume True volume depletion ● Can be caused by vomiting, NGT suctioning, diuretic use, blood loss, loss of blood into 3rd space and marked sweat loss(CF). ● Corrected by volume expansion by isotonic saline ● Treatment of concomitant hypokalemia 04/01/2025 64
Cont’d Reduced effective arterial blood volume (edematous state) ● Metabolic alkalosis occur due to diuretic therapy and hypokalemia as complication of diuretic therapy. ● Volume replacement has no role. ● Acetazolamide is the preferred diuretics. ○ Carbonic anhydrase inhibitor. ○ Dose = 125-250 mg po daily or twice daily. ○ Mechanism – inhibit proximal NaHCO3 reabsorption and increase HCO3 excretion. ○ Exacerbates hypokalemia. 04/01/2025 65
Cont’d 2. Chloride depletion ● Volume expansion with chloride containing salts 3. Potassium depletion ● Correction of Hypokalemia with Potassium chloride. 4. Renal failure ● Hemodialysis against a dialysate low in [HCO3] and high in [Cl– ] can be effective when renal function is impaired. 04/01/2025 66
Cont’d Which group of patients are treated with HCL?  Severe metabolic alkalosis (HCO3 >50meq/l or PH>7.55.  Pts with renal insufficiency who can’t be dialyzed. 04/01/2025 67
RESPIRATORY ACIDOSIS • Respiratory acidosis is the acid-base disturbance initiated by an increase in CO2 tension (Pco2) of body fluids and whole-body CO2 stores • The level of PaCO2 is determined by the of two factors, the rate of carbon dioxide production (VCO2) and the rate of alveolar ventilation (VA) • Its main elements are the respiratory pump, which generates a pressure gradient responsible for airflow, and the loads that oppose such action. • CO2 retention can occur from an imbalance between the strength of 04/01/2025 68
Respiratory acidosis 04/01/2025 69
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Secondary physiologic response ●In acute respiratory acidosis, there is a compensatory elevation in HCO3 − (due to cellular buffering mechanisms) that increases 1 mmol/L for every 10-mmHg increase in Paco2. ●In chronic respiratory acidosis (>24 h), renal adaptation increases the 04/01/2025 72
Chronic adaptation renal regulation mechanisms It requires 3-5 days of sustained hypercapnia for completion. A transient increase in urinary net acid excretion  persistent ,increase in the rate of renal bicarbonate reabsorption plasma HCO3 - ↑0.4 mEq/L for each mm Hg chronic increment in PaCO2; 04/01/2025 73
Clinical presentation  Varies according to the severity and duration of respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia.  Systemic vasodilalatation (most obvious in cerebral circulation, direct relation to the level of Paco2)  CO2 retention (whether acute or chronic) is always associated with hypoxemia in patients breathing room air. 04/01/2025 74
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Diagnosis ● ABG analysis;↑ PaCO2 (>45 mmhg)arterial pH <7.35 ↓ ● A detailed history and physical examination may indicate the cause. ● For pulmonary causes, pulmonary function studies including spirometry, diffusion capacity for CO, lung volumes and arterial Paco2 and O2 saturation ● For non-pulmonary causes, a detailed drug history, measurement of hematocrit, and assessment of upper airway, chest wall, pleura and neuromuscular 04/01/2025 76
TREATMENT Respiratory Acidosis Depends on its severity and rate of onset  Reverse the underlying cause and alveolar ventilation  Oxygen administration  Ventilatory Support (NIPPV vs invasive)  Avoide aggressive and rapid correction of hypercapnia  provide sufficient Cl and K+ to enhance the renal − excretion of HCO3 . − 04/01/2025 77
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RESPIRATORY ALKALOSIS  Respiratory alkalosis is the acid-base disturbance initiated by a reduction in PaCO2.  Develops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production by the tissues.  It is the most common acid-base abnormality in critically ill patients  Is an adverse prognostic sign, especially if Paco2 is below 20 to 25 mm Hg 04/01/2025 80
Secondary physiologic response/ adaptation ○The compensatory response to acute respiratory alkalosis reduces the HCO3 conc. by 2 meq/l for every 10 mmhg decline in the PCO2 ○If the reduced PCO2 persists for more than 3-5 days, then the disorder is considered chronic & the serum HCO3 conc. should fall by 4-5 meq/l for every 10 mmhg reductin in the PCO2 04/01/2025 81
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Clinical manifestation • Depends the severity and duration but primarily underlying disease. 1. Neurological: Rapid decrements in PaCO2 to half the normal values or lower are typically accompanied by  paresthesias of the extremities,  chest discomfort,  circumoral numbness, lightheadedness,  confusion, and infrequently, tetany or generalized seizures. These manifestations are seldom present in 04/01/2025 83
cardiovascular  No appreciable changes in CO,BP or cardiac rhythm occur in actively hyperventilating subjects.  major reductions in cardiac output and blood pressure, and substantial hyperlactatemia frequently occur in passively hyperventilating ( MV ).  patients with CAD might suffer hypocapnia-induced coronary vasoconstriction, resulting in angina pectoris and arrhythmias. 04/01/2025 84
Diagnosis ●ABG analysis ↑PH (7.45) PCO2 < 35 mmhg ↓ ↓ HCO3 - ●patient history, physical examination, and ancillary laboratory ●Plasma K + is often reduced and the Cl- is increased. 04/01/2025 85
Treatment ● The management of respiratory alkalosis is directed toward alleviation of the underlying disorder. ● Respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the stimulus is controlled. ● Avoid rapid correction vasodilation of ischemic areas, resulting in → reperfusion injury in the brain & lung. ● Mechanically ventilated patients adjust tidal volume rate, sedation and pain control 04/01/2025 86
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Mixed ABD  Refers to the presence of two or more independent acid base disorders.  Evaluation of ABD initially require identification of the major disorder and determination of the degree of compensation  Inappropriate compensation suggests a second 04/01/2025 88
Recap 04/01/2025 89
To check for compensation Primary Disorder Expected Compensation pH Metabolic Acidosis Winter’s Formula pCO2 = 1.5 [HCO3] + 8 +/- 2 Metabolic Alkalosis Summer’s Formula pCO2 = 0.7 [HCO3] + 20 +/- 5 Respiratory Acidosis Acute [HCO3] rises by 1 for every 10 mm Hg increase in pCO2 Expect pH decrease 0.08 for every 10 mmHg increase in PCO2 Chronic [HCO3] rises by 4 for every 10 mm Hg increase in pCO2 Expected pH do decrease 0.03 for every 10 mmHg increase in PCO2 Respiratory Alkalosis Acute [HCO3] decreases by 2 for every 10 mm Hg decrease in pCO2 Expect pH increase 0.08 for every 10 mmHg decrease in PCO2 Chronic [HCO3] decreases by 5 for every 10 mm Hg decrease in pCO2 Expected pH to increase 0.02 for every 10 mmHg decrease in pCO2 04/01/2025 90
Steps for ABG analysis 1. What is the pH? Acidemia or Alkalemia? 2. What is the primary disorder present? 3. Is there appropriate compensation? 4. Is the compensation acute or chronic? 5. Is there an anion gap? 6. If there is a AG check the delta gap? 7. What is the differential for the clinical processes?
Step 5: Calculate the anion gap  AG used to assess acid-base status in metabolic acidosis   AG &  HCO3 - used to assess mixed acid-base disorders  AG based on principle of electroneutrality:  Total Serum Cations = Total Serum Anions  Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids)  Na + UC = HCO3 + Cl + UA  Na – (HCO3 + Cl) = UA – UC  Na – (HCO3 + Cl) = AG  Normal =12 ± 4
Influence of Albumin ● Note that albumin is the principal unmeasured anion, and the principal determinant of the anion gap. ● Hypoalbuminemia lowers the AG
Cont...  The AG can be adjusted for low albumin levels by using the following formula  AG corrected = AG + 2.5[4 – albumin]  (4 represents the normal concentration of albumin in plasma).  If there is an anion Gap then calculate the Delta/delta gap (step 6) to determine additional hidden nongap metabolic acidosis or metabolic alkalosis  If there is no anion gap then start analyzing for non-anion gap acidosis
Case  Calculate Anion gap • ABG :PH 7.23/ PCO217/ HCO- 3 7 • BMP: Na 123/ Cl 97/BUN 119/ Cr 5.1/Albumin 2  AG = Na – Cl – HCO3 (normal 12 ± 4) ○ 123 – 97 – 7 = 19  AG corrected = AG + 2.5[4 – albumin] ● = 19 + 2.5 [4 – 2] ● = 19 + 5 = 24
Step6:CalculateDeltaGap ● The delta-delta ● The ratio of ΔAG/Δ[HCO3] ● Used in anion gap metabolic acidosis. ● This would reveal additional METABOLIC disorder. ● You can have an anion gap metabolic acidosis ○ Plus a non-AG metabolic acidosis ○ OR ○ Plus a metabolic alkalosis!
Delta-Delta ● The ratio of ΔAG/Δ[HCO3]. ■ AG-normal AG/ normal [HCO3] – [HCO3] ● Using 12 as normal AG, and 24 as normal [HCO3] ■ AG-12/24- [HCO3] ● If ratio of ΔAG/Δ[HCO3] is…. ○ >2 : metabolic alkalosis is present. ○ 1-2: no other metabolic disorder. ○ <1: additional non-anion gap metabolic acidosis
Delta-delta made simple ● Step 1: calculate the ΔAG ● Step 2: add the ΔAG to the current [HCO3-] ● Step 3: compare this new [HCO3-] to the normal range of 22-28. ○ <22additional non-AG metabolic acidosis is present ○ >28additional metabolic ALKALOSIS is present. ○ 22-28: no additional metabolic disorder
cases 04/01/2025 99
Answer  The patient has high Ph- alkalemia  The pco2 is high(respiratory acidosis) and the bicarbonate is high  (metabolic alkalosis)  The high Ph and high bicarbonate tell us the metabolic alkalosis is the primary process  The AG-10,normal value  Summary:a primary metabolic alkalosis with respiratory compensation 04/01/2025 100
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Answer  The patient has a low pH  The patient has a high pco2(respiratory acidosis) and a high bicarbonate (metabolic alkalosis).  The combination of low pH and high pco2 tells us that the respiratory acidosis is the primary process  Summary: primary respiratory acidosis with compensatory metabolic alkalosis 04/01/2025 102
04/01/2025 103
answer  The patient has a very low pH(acidemia)  The patient has a low pcow(respiratory alkalosis) and a very low bicarbonate (metabolic acidosis).  The low pH in conjunction with the low bicarbonate tells us the metabolic acidosis is the primary process  The AG is elevated at 30- high AG MA  The respiratory alkalosis is the compensatory process,although despite a huge increase in Minute ventilation the patient still has a very low ph 04/01/2025 104
Cont…  The delta gap is 30-12=18 and the delta delta is 18+2=20.  since the delta delta is below 22,we know that there is additional non gap metabolic acidosis as well  Summary: combined elevated anion gap and non gap metabolic acidosis with compensatory respiratory alkalosis 04/01/2025 105
04/01/2025 106
Answer  The patient has a low pH(acidemia)  The pco2 is low ((respiratory alkalosis) and the bicarbonate is low(metabolic acidosis)  The combination of low pH and the low bicarbonate tells us that the metabolic acidosis is the primary process  The anion gap is elevated at 24.This tells us the patient has a primary high AG MA  The delta gap is 24-12=12. The delta delta is 12+17=29.because the Del- Del is greater than 26,we know the patient has a concurrent metabolic alkalosis  Summary: Primary elevated anion gap metabolic acidosis with respiratory compensation and a concurrent metabolic alkalosis 04/01/2025 107
Case 3 ● 42 year old man experienced crushing substernal chest pain and diaphoresis and shortness of breath and was brought to the emergency room. ○ Vital signs: BP 70/50 HR 110 RR 14 ○ Arterial blood gas analysis on room air: ○ pH 7.32/PCO2 24 mmHg/PO2 88 mm Hg/ HCO3ֿ 12 mEq/l /SaO2 96% ● Serum electrolytes: ○ Na 135 mEq/l K 5.4 mEq/l Cl 101 mEq/l , Lactate 12 mEq/l 04/01/2025 108
Answer • Acidosis • Metabolic acidosis • Over-compensated • High anion gap • Delta/delta <1 • Respiratory alkalosis ans aditional non anaion gap acidosis • Primary high anion gap metabolic acidosis with secondary repiratory alkalosis and aditional non anion gap metabolic acidosis 04/01/2025 109
References 04/01/2025 110
04/01/2025 111

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Seminar on acid base disorders nephrolog

  • 1.
    Moderator Dr Nebiyu(Internist, Consultant Nephrologist) Presenters Dr Yoseph (R1) Dr Bisrat(R2) July 16,2024 ACID BASE DISORDERS
  • 2.
    Outline ●Basic concepts ●Arterial bloodgas analysis ●Metabolic acidosis ●Metabolic alkalosis ●Respiratory acidosis ●Respiratory alkalosis ●Case discussion 04/01/2025 2
  • 3.
    Basic concepts ● Acid-basedisorder; change in normal value of extracellular PH that results when renal or respiratory function is abnormal or when acid or base load over whelms excretory capacity. ● Acidemia-decrease in blood PH below normal range (<7.35) • Acidosis-is process that increases H+ by increasing pco2 or decreasing HCO3 − ● Alkalemia-elevation of blood PH above normal range(>7.45) 04/01/2025 3
  • 4.
  • 5.
    Cont... ● Respiratory acidosis-A disorder that elevates PaCO2 & reduces PH ● Respiratory alkalosis- A disorder that reduces PaCO2 & elevates PH ● Metabolic acidosis- A disorder that reduces HCO- 3 & PH ● Metabolic alkalosis- A disorder that elevates HCO- 3 & PH ● Simple acid-base disorder- The presence of one of the above disorders with the appropriate respiratory or renal compensation. ● Mixed acid-base disorder- The simultaneous presence of more than one acid-base disorder. 04/01/2025 5
  • 6.
  • 7.
    7 Arterial PH ismaintained by 3 regulatory mechanisms 04/01/2025
  • 8.
    RESPIRATORY REGULATORY MECHANISM ●Regulate PaCo2 in association with CNS (medullary chemo receptors) to defend PH  During metabolic alkalosis→ ↓ventilation(PaCo2 ↑)  During metabolic acidosis→ ↑ventilation(PaCo2↓) 04/01/2025 8
  • 9.
    RENAL REGULATORY MECHANISM 3 mechanisms I. Reabsorption of filtered HCO3 - II. Excreation of NH4 in urine III. Formation of titrable acid 04/01/2025 9
  • 10.
    ABG ANALYSIS ● ABGis a test that measures PH/PaCO2/PaO2/ SaO2/HCO3 concentration on arterial blood ● Used for:- ○ Identification and monitoring of acid-base disturbances ○ Measurement of PaO2 and PaCO2 ○ Assessment of the response to therapeutic interventions(eg, Insulin in DKA) ○ Detection and quantification of the levels of abnormal hemoglobin ○ Procurement of a blood sample in an acute emergency when venous sampling is not feasible. 04/01/2025 10
  • 11.
    Absolute ● An abnormalmodified Allen's test ● Local infection or distorted anatomy at the puncture site, ● Severe peripheral vascular disease of the artery selected for sampling ● Active Raynaud's Relative ● Supra therapeutic coagulopathy (INR 3, aptt 100 ≥ ≥ seconds and infusion of thrombolytic agents ● A platelet count <50 x 109 Contraindications for ABG sampling 04/01/2025 11
  • 12.
  • 13.
  • 14.
  • 15.
    Arterial Vs VenousGas Analysis VALUES ARTERIAL BLOOD VENOUS BLOOD PH 7.4(7.35-7.45) 7.36(7.31-7.41) PaO2 80-100 mmHg 35-40 mmHg O2 SATURATION 95% 70-75% PaCo2 35-45 41-51 HCO3 22-26 22-26 BASE EXCESS -2 to +2 -2 to +2 04/01/2025 15
  • 16.
    Metabolic Acidosis ● Metabolicacidosis is defined as a pathologic process that, when unopposed, increases the concentration of H+ in the body and reduces HCO3. ○ ↓PH,↓HCo3,↓PaCo2 ● Mechanisms ○ ↑ Acid production ○ Loss of bicarbonate ○ ↓ Renal acid excretion ○ Dilutional acidosis 04/01/2025 16
  • 17.
    Cont’d ● The serumanion gap can be used to categorize MA into two groups ○ High anion gap MA ○ Normal anion gap MA ● Blood cations(+ve) must be balanced with anions(-ve) to maintain electroneutrality ○ but when comparing main anions(Cl-,HCo3-) with main cations (Na+,K+),there is shortage of anions this is termed ANION GAP, which is 10-14(use 12 as absolute value) 04/01/2025 17
  • 18.
    Cont’d ● This gapis due to anions which are difficult to measure(SO4-, pO4-, - vely charged proteins). ○ Anion Gap = Na - (Cl + HCo3) ○ Use 12 as an absolute value for AG ○ ↓1gm/dl albumin = add 2.5mmol to the Anion Gap  Corrected serum anion gap = (Serum anion gap measured) + (2.5 x [4.5 - Observed serum albumin]) ● An increase in the AG is most often due to an increase in unmeasured anions and, less commonly, may be due to a decrease in unmeasured cations (calcium, magnesium, potassium).  a serum potassium of 6 mEq/L will reduce the anion gap by 2 mEq/L 04/01/2025 18
  • 19.
    Special Scenarios ● Adecrease in the AG can be due to 1. The addition to the blood of abnormal cations, 2. A reduction in the plasma albumin 3. A decrease in the effective anionic charge on albumin by acidosis; 4. Hyperviscosity and severe hyperlipidemia. 04/01/2025 19
  • 20.
  • 21.
  • 22.
    22 Clinical features  Profoundeffect on nervous, respiratory and cardiac system.  Depressed CNS (lethargy, stupor, coma), headache  Increased ventilation (Kussmaul breathing)  Depressed cardiac contractility but normal inotropic function due to catecholamine release  Peripheral vasodilation, central vasoconstriction  Predisposed to pulmonary edema with minimal fluid due to low pulmonary vasculature compliance  Glucose intolerance 04/01/2025
  • 23.
    Respiratory compensation  Thedevelopment of metabolic acidosis will normally generate a compensatory respiratory response  With normal respiratory compensation, Pco2 decreases by 1.2 mm Hg for every 1 mEq/L net decrease in [HCO3–]. 04/01/2025 23
  • 24.
    Cont’d  PCO2 =(1.5 x HCO3 + 8) ± 2.  This equation, which is called Winter’s formula, was derived in children, half of whom were between two months and two years of age.  PCO2 = HCO3 + 15.  The PCO2 should approximate the decimal digits of the arterial pH. 04/01/2025 24
  • 25.
    Cont….  These ruleswork well for mild to moderately severe metabolic acidosis (HCO3 between 7 and 22 mEq/L).  For more severe metabolic acidosis (HCO3 less than 7 mEq/L), the pCO2 should be maximally reduced to the 8 to 12 mmHg range.  As an example: pH = 7.30; pCO2 = 30 mmHg (4.0 kPa); 04/01/2025 25
  • 26.
    The delta aniongap/ delta HCO3 ratio in high anion gap MA  When the AG increases in magnitude as a result of metabolic acidosis, that increase should be compared with the magnitude of the fall in HCO3.  This represents the delta AG/delta HCO3 ratio.  Opposite changes in the serum AG and HCO3 concentration would result in a delta AG/delta HCO3 ratio of 1:1 04/01/2025 26
  • 27.
    Cont'd  A deltaAG/delta HCO3 ratio below 1 suggests one of the following:  A coexisting normal AG metabolic acidosis .  A high AG acidosis in which both renal function is preserved and the acid anion is readily excreted into the urine  Patients with renal tubular acidosis of early renal insufficiency  A delta AG/delta HCO3 ratio of 1:1 is consistent with an 04/01/2025 27
  • 28.
    Cont'd  A deltaAG/delta HCO3 ratio between 1 and 2 generally occurs with high AG metabolic acidosis, such as lactic acidosis, when renal function is reduced and the acid anions are, thereby, all retained in the body. Metabolic alkalosis coexists with a high AG metabolic acidosis or  When the baseline HCO3 level is elevated as a result of chronic respiratory acidosis. 04/01/2025 28
  • 29.
    Cont'd ● Delta AG/deltaHCO3 ratio above 2 usually suggests that metabolic alkalosis coexists with a high AG metabolic acidosis or that the baseline HCO3 level is elevated as a result of chronic respiratory acidosis. 04/01/2025 29
  • 30.
    Renal vs Extrarenalcauses of MA  Renal and extrarenal causes of metabolic acidosis can be distinguished by measuring urinary ammonia excretion.  Because most laboratories do not measure urinary ammonia, one can indirectly assess ammonia excretion by measuring the urinary anion gap (UAG). 04/01/2025 30
  • 31.
  • 32.
    Renal tubular acidosis In RTA metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.  All forms of RTA are characterized by a normal anion gap (hyperchloremic) metabolic acidosis. 04/01/2025 32
  • 34.
  • 35.
    Treatment of MA ●General approach ○ Reverse the underlying pathophysiologic mechanism ○ General vs specific approach ○ Consider acute and chronic forms of MA separately ● Acute MA ○ Alkali therapy ■ Severe acidemia with pH<7.1 ■ pH 7.1-7.2 with severe acute kidney injury (ie, a twofold or greater increase in serum creatinine or oliguria) 04/01/2025 35
  • 36.
  • 37.
    Chronic MA  Themost common causes of chronic metabolic acidosis are diarrhea, advanced chronic kidney disease, and the various forms of RTA  Alkali therapy  Consider benefits of therapy The rational for alkali therapy is summarized here:  Increasing the bicarbonate concentration reduces or eliminates the need for compensatory hyperventilation and can alleviate the dyspnea experienced by some patients.  Chronic metabolic acidosis may have adverse effects on muscle function and metabolism, skeletal integrity, hormone levels, and other physiologic parameters. In children, for example, correction of chronic metabolic acidosis restores skeletal growth 04/01/2025 37
  • 38.
    Cont…  Patients withchronic distal (type 1) RTA are likely to develop nephrocalcinosis and calcium-containing kidney stones. This defect can be reversed with adequate bicarbonate replacement.  Chronic metabolic acidosis in patients with kidney dysfunction may accelerate the progression of their kidney damage, and reversal of the acidosis can slow this process 04/01/2025 38
  • 39.
    Dosing of alkalitherapy (when given) ● Ampules of hypertonic sodium bicarbonate are available as 8.4 percent (50 mEq/50 mL), 7.5 percent (44.6 mEq/50 mL), and 4.2 percent solutions (25 mEq/50 mL).  Acute metabolic acidosis ● The initial goal is a pH >7.2 and/or serum bicarbonate concentration >16 mEq/L. ● Infuse 2 ampules (100 mL) of 7.5 percent sodium bicarbonate (44.6 mEq/50 mL) over 1 to 2 minutes and remeasure the blood pH and serum bicarbonate concentration (eg, after two hours). ● If the distribution space is approximately 55 percent of the body weight (as it is in healthy individuals), the serum bicarbonate level should increase by approximately 2 to 3 mEq/L. 04/01/2025 39
  • 40.
    Cont..  Chronic metabolicacidosis – When chronic alkali treatment is required, options include the sodium or potassium salts of either bicarbonate or a metabolizable anion such as citrate or lactate  The potassium salts are indicated when hypokalemia and total body potassium deficits exist. In general, the initial dose is 50 to 100 mEq per day, which is then titrated up, or down, as required.  If ongoing bicarbonate losses persist or accelerate, the dose will need to be adjusted accordingly 04/01/2025 40
  • 41.
    Cont’d Treatment goal  Increase[HCO3] to 10-12mmol/L and the PH to 7.20 ● Preferred alkali is NaHCO3 ○ HCO3 deficit= HCO3 space * HCO3 deficit/L ○ HCO3 space= (0.4 + (2.6/HCO3)) * lean body weight 04/01/2025 41
  • 42.
    42 Lactic Acidosis  Lactateis an end product in glucose metabolism  Formed by reduction of pyruvate catalyzed by LDH  Principal sites of production are skeletal muscle (25%), skin (25%), red blood cells (20%), brain (20%), and intestine (10%).  Activated neutrophils are an additional source of lactate in inflammatory conditions like ARDS  The concentration of lactate in plasma is usually 2 mmol/L, with a lactate:pyruvate ratio of 10:1  Lactate is cleared from plasma by the liver (60%), kidneys (30%), and heart (10%). 04/01/2025
  • 43.
    43 Lactic Acidosis ● Themost common cause of metabolic acidosis in hospitalized patients ● Lactate level >2mmol/L –hyperlactatemia ● Lactate level > 4mmol/L – lactic acidosis ● D-Lactic acid acidosis – formed by gut bacteria ● L-lactic acid acidosis ○ Type A ○ Type B 04/01/2025
  • 44.
    44 Type A –hypoxic (Poor tissue perfusion) ● Circulatory insufficiency (septic/hypovolemic shock, heart failure, mesenteric ischemia) ● Severe anemia ● Mitochondrial enzyme deficiency ● Inhibitors (carbon monoxide, cyanide) 04/01/2025
  • 45.
    45 Type B –non hypoxic (aerobic disorders) ● Severe infections (malaria, cholera) ● Renal failure ● Hepatic failure ● Seizure ● Thiamine deficiency Drugs/toxins ● NRTIs ● Metformin – primarily in renal insufficiency. Treated with dialysis ● Isoniazid ● Fructose ● Acetaminophen depletes glutathione  pyroglutamic acidemia in critical illness ● Ethanol, methanol, propylene glycol 04/01/2025
  • 46.
    46 L-Lactic acidosis treatment ●Correct underlying cause. ● Restore tissue perfusion ● Alkali therapy for severe, acute academia ○ Alkali therapy if indicated(Severe acidemia (PH<7.00) to improve cardiovascular function.)  Therapeutic goal ● To raise arterial PH to no more than 7.2 or the [HCO3] to no more than 12meq/L over 30-40mins ○ HCO3 not an effective buffer unless pH is very low ○ NaHCO3 may worsen acidosis by stimulating lactate production (phosphofructokinase) ○ Overshoot alkalosis (lactate is converted to bicarbonate) ○ It is a CO2 burden that must be removed by the lungs. Carbicarb is a commercially available buffer solution that is a 1:1 mixture of sodium bicarbonate and disodium 04/01/2025
  • 47.
    Cont’d ● DKA= standardDKA mx ● Alcoholic ketoacidosis ○ Fluid replacement therapy with saline and 5% dw ○ Corection of electrolyte disturbance ● GI bicarbonate loss ○ Treat the cause ○ Volume replacement and alkali therapy when indicated 04/01/2025 47
  • 48.
    Reverse/prevents ● Reduced leftventricular contractility ● Arrhythmias ● Arterial vasodilation ● Impaired responsiveness to catecholamine Potential harms of bicarbonate therapy ● Increased arterial and tissue capillary PCO2 ● Acceleration of lactate generation ● Reduced ionized calcium ● Hypernatremia ● Extracellular fluid volume expansion Benefits of HCO3 therapy 04/01/2025 48
  • 49.
    Cont’d ● CKD ○ Currentlythe 2013 Kidney Disease Improving Global Outcomes (KDIGO) guidelines recommended that, in patients with CKD and metabolic acidosis, alkali therapy be used to maintain the [HCO3] in the normal range (23 to 29 meq/L). ○ Renal replacemnt therapy ● RTA ○ Maintenance of normokalemia ○ Alkali therapy with sodium and potassium citrate ○ Mineralocorticoid therapy ○ Diuretic therapy 04/01/2025 49
  • 50.
    Classic distal RTA ●Administration of NaHCO3 or sodium citrate with a goal of correcting the HCO3 to normal level. ● Concomitant administration of potassium in acutely acidotic patients with hyopkalemia. ● Alkali therapy decrease frequency of nephrocalcinosis, improve bone density and resume normal growth pattern in children. Generalized distal RTA ● Restore normokalemia. 04/01/2025 50
  • 51.
    Metabolic Alkalosis  Metabolicalkalosis is caused by retention of excess alkali and is characterized by ↑PH, HCo3, PaCo2 ↑ ↑  Hypoventilation, producing a secondary increase in arterial Pco2. 04/01/2025 51
  • 52.
    ● Three factorsplay key roles: ○ Chloride depletion ○ Abnormal aldosterone secretion, and ○ Hypokalemia. 04/01/2025 52 Cont’d
  • 53.
  • 54.
  • 55.
  • 56.
  • 57.
    Features ● The mostimportant adverse effect is hypokalemia,which increase the likelihood of cardiac arrythmia(esp. in pts with underlying cardiac dysfunction) ● Usually pts with Hco3 level up to 40mmol/l can be assymptomatic but when > 50 mmol/l may develop seizures,tetany,delirium or stupor. 04/01/2025 57
  • 58.
    Respiratory compensation ● ThePCO2 raises by 0.7mmHg for every 1mEq/L elevation in serum HCO3 concentration ○PCO2=HCO3 + 10 ○PCO2 = 40 + 0.7 × ([HCO3 ] 24) − 04/01/2025 58
  • 59.
    Diagnosis ● Diagnosis ofmetabolic alkalosis involves three steps. ● The first step ○ Detection, is most often based on the finding of elevated venous [total CO2]. ● The second step ○ evaluation of the secondary response (hypoventilation), excluding the possibility that a respiratory acid-base abnormality is also present. ○ This step requires measurement of arterial pH and Pco2. ● The third step ○ Determination of the cause 04/01/2025 59
  • 60.
    Cont’d ●Serum [total CO2]levels above 30 mmol/l in association with hypokalemia are virtually pathognomonic of metabolic alkalosis. 04/01/2025 60
  • 61.
  • 62.
    Treatment  What isthe cause of excessive serum HCO3 concentration?  Why is the excess HCO3 not excreted through the urine? 04/01/2025 62
  • 63.
    Treating factors thatincrease HCO3 production GI H+ loss - PPIs or H2-blockers - Reduce gastric suctioning Intracellular H+ shift - Correction of hypokalemia Exogenous alkali administration - Discontinue all alkali including Na+ and K+ salts of any organic anion that will later be metabolized to HCO3 Excessive Renal H+ loss - Discontinue diuretics. 04/01/2025 63
  • 64.
    Treating factors thatimpair renal excretion of HCO3 1. Reduced arterial blood volume True volume depletion ● Can be caused by vomiting, NGT suctioning, diuretic use, blood loss, loss of blood into 3rd space and marked sweat loss(CF). ● Corrected by volume expansion by isotonic saline ● Treatment of concomitant hypokalemia 04/01/2025 64
  • 65.
    Cont’d Reduced effective arterialblood volume (edematous state) ● Metabolic alkalosis occur due to diuretic therapy and hypokalemia as complication of diuretic therapy. ● Volume replacement has no role. ● Acetazolamide is the preferred diuretics. ○ Carbonic anhydrase inhibitor. ○ Dose = 125-250 mg po daily or twice daily. ○ Mechanism – inhibit proximal NaHCO3 reabsorption and increase HCO3 excretion. ○ Exacerbates hypokalemia. 04/01/2025 65
  • 66.
    Cont’d 2. Chloride depletion ●Volume expansion with chloride containing salts 3. Potassium depletion ● Correction of Hypokalemia with Potassium chloride. 4. Renal failure ● Hemodialysis against a dialysate low in [HCO3] and high in [Cl– ] can be effective when renal function is impaired. 04/01/2025 66
  • 67.
    Cont’d Which group ofpatients are treated with HCL?  Severe metabolic alkalosis (HCO3 >50meq/l or PH>7.55.  Pts with renal insufficiency who can’t be dialyzed. 04/01/2025 67
  • 68.
    RESPIRATORY ACIDOSIS • Respiratoryacidosis is the acid-base disturbance initiated by an increase in CO2 tension (Pco2) of body fluids and whole-body CO2 stores • The level of PaCO2 is determined by the of two factors, the rate of carbon dioxide production (VCO2) and the rate of alveolar ventilation (VA) • Its main elements are the respiratory pump, which generates a pressure gradient responsible for airflow, and the loads that oppose such action. • CO2 retention can occur from an imbalance between the strength of 04/01/2025 68
  • 69.
  • 70.
  • 71.
  • 72.
    Secondary physiologic response ●Inacute respiratory acidosis, there is a compensatory elevation in HCO3 − (due to cellular buffering mechanisms) that increases 1 mmol/L for every 10-mmHg increase in Paco2. ●In chronic respiratory acidosis (>24 h), renal adaptation increases the 04/01/2025 72
  • 73.
    Chronic adaptation renalregulation mechanisms It requires 3-5 days of sustained hypercapnia for completion. A transient increase in urinary net acid excretion  persistent ,increase in the rate of renal bicarbonate reabsorption plasma HCO3 - ↑0.4 mEq/L for each mm Hg chronic increment in PaCO2; 04/01/2025 73
  • 74.
    Clinical presentation  Variesaccording to the severity and duration of respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia.  Systemic vasodilalatation (most obvious in cerebral circulation, direct relation to the level of Paco2)  CO2 retention (whether acute or chronic) is always associated with hypoxemia in patients breathing room air. 04/01/2025 74
  • 75.
  • 76.
    Diagnosis ● ABG analysis;↑PaCO2 (>45 mmhg)arterial pH <7.35 ↓ ● A detailed history and physical examination may indicate the cause. ● For pulmonary causes, pulmonary function studies including spirometry, diffusion capacity for CO, lung volumes and arterial Paco2 and O2 saturation ● For non-pulmonary causes, a detailed drug history, measurement of hematocrit, and assessment of upper airway, chest wall, pleura and neuromuscular 04/01/2025 76
  • 77.
    TREATMENT Respiratory Acidosis Dependson its severity and rate of onset  Reverse the underlying cause and alveolar ventilation  Oxygen administration  Ventilatory Support (NIPPV vs invasive)  Avoide aggressive and rapid correction of hypercapnia  provide sufficient Cl and K+ to enhance the renal − excretion of HCO3 . − 04/01/2025 77
  • 78.
  • 79.
  • 80.
    RESPIRATORY ALKALOSIS  Respiratoryalkalosis is the acid-base disturbance initiated by a reduction in PaCO2.  Develops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production by the tissues.  It is the most common acid-base abnormality in critically ill patients  Is an adverse prognostic sign, especially if Paco2 is below 20 to 25 mm Hg 04/01/2025 80
  • 81.
    Secondary physiologic response/adaptation ○The compensatory response to acute respiratory alkalosis reduces the HCO3 conc. by 2 meq/l for every 10 mmhg decline in the PCO2 ○If the reduced PCO2 persists for more than 3-5 days, then the disorder is considered chronic & the serum HCO3 conc. should fall by 4-5 meq/l for every 10 mmhg reductin in the PCO2 04/01/2025 81
  • 82.
  • 83.
    Clinical manifestation • Dependsthe severity and duration but primarily underlying disease. 1. Neurological: Rapid decrements in PaCO2 to half the normal values or lower are typically accompanied by  paresthesias of the extremities,  chest discomfort,  circumoral numbness, lightheadedness,  confusion, and infrequently, tetany or generalized seizures. These manifestations are seldom present in 04/01/2025 83
  • 84.
    cardiovascular  No appreciablechanges in CO,BP or cardiac rhythm occur in actively hyperventilating subjects.  major reductions in cardiac output and blood pressure, and substantial hyperlactatemia frequently occur in passively hyperventilating ( MV ).  patients with CAD might suffer hypocapnia-induced coronary vasoconstriction, resulting in angina pectoris and arrhythmias. 04/01/2025 84
  • 85.
    Diagnosis ●ABG analysis ↑PH(7.45) PCO2 < 35 mmhg ↓ ↓ HCO3 - ●patient history, physical examination, and ancillary laboratory ●Plasma K + is often reduced and the Cl- is increased. 04/01/2025 85
  • 86.
    Treatment ● The managementof respiratory alkalosis is directed toward alleviation of the underlying disorder. ● Respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the stimulus is controlled. ● Avoid rapid correction vasodilation of ischemic areas, resulting in → reperfusion injury in the brain & lung. ● Mechanically ventilated patients adjust tidal volume rate, sedation and pain control 04/01/2025 86
  • 87.
  • 88.
    Mixed ABD  Refersto the presence of two or more independent acid base disorders.  Evaluation of ABD initially require identification of the major disorder and determination of the degree of compensation  Inappropriate compensation suggests a second 04/01/2025 88
  • 89.
  • 90.
    To check forcompensation Primary Disorder Expected Compensation pH Metabolic Acidosis Winter’s Formula pCO2 = 1.5 [HCO3] + 8 +/- 2 Metabolic Alkalosis Summer’s Formula pCO2 = 0.7 [HCO3] + 20 +/- 5 Respiratory Acidosis Acute [HCO3] rises by 1 for every 10 mm Hg increase in pCO2 Expect pH decrease 0.08 for every 10 mmHg increase in PCO2 Chronic [HCO3] rises by 4 for every 10 mm Hg increase in pCO2 Expected pH do decrease 0.03 for every 10 mmHg increase in PCO2 Respiratory Alkalosis Acute [HCO3] decreases by 2 for every 10 mm Hg decrease in pCO2 Expect pH increase 0.08 for every 10 mmHg decrease in PCO2 Chronic [HCO3] decreases by 5 for every 10 mm Hg decrease in pCO2 Expected pH to increase 0.02 for every 10 mmHg decrease in pCO2 04/01/2025 90
  • 91.
    Steps for ABGanalysis 1. What is the pH? Acidemia or Alkalemia? 2. What is the primary disorder present? 3. Is there appropriate compensation? 4. Is the compensation acute or chronic? 5. Is there an anion gap? 6. If there is a AG check the delta gap? 7. What is the differential for the clinical processes?
  • 92.
    Step 5: Calculatethe anion gap  AG used to assess acid-base status in metabolic acidosis   AG &  HCO3 - used to assess mixed acid-base disorders  AG based on principle of electroneutrality:  Total Serum Cations = Total Serum Anions  Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids)  Na + UC = HCO3 + Cl + UA  Na – (HCO3 + Cl) = UA – UC  Na – (HCO3 + Cl) = AG  Normal =12 ± 4
  • 93.
    Influence of Albumin ●Note that albumin is the principal unmeasured anion, and the principal determinant of the anion gap. ● Hypoalbuminemia lowers the AG
  • 94.
    Cont...  The AGcan be adjusted for low albumin levels by using the following formula  AG corrected = AG + 2.5[4 – albumin]  (4 represents the normal concentration of albumin in plasma).  If there is an anion Gap then calculate the Delta/delta gap (step 6) to determine additional hidden nongap metabolic acidosis or metabolic alkalosis  If there is no anion gap then start analyzing for non-anion gap acidosis
  • 95.
    Case  Calculate Aniongap • ABG :PH 7.23/ PCO217/ HCO- 3 7 • BMP: Na 123/ Cl 97/BUN 119/ Cr 5.1/Albumin 2  AG = Na – Cl – HCO3 (normal 12 ± 4) ○ 123 – 97 – 7 = 19  AG corrected = AG + 2.5[4 – albumin] ● = 19 + 2.5 [4 – 2] ● = 19 + 5 = 24
  • 96.
    Step6:CalculateDeltaGap ● The delta-delta ●The ratio of ΔAG/Δ[HCO3] ● Used in anion gap metabolic acidosis. ● This would reveal additional METABOLIC disorder. ● You can have an anion gap metabolic acidosis ○ Plus a non-AG metabolic acidosis ○ OR ○ Plus a metabolic alkalosis!
  • 97.
    Delta-Delta ● The ratioof ΔAG/Δ[HCO3]. ■ AG-normal AG/ normal [HCO3] – [HCO3] ● Using 12 as normal AG, and 24 as normal [HCO3] ■ AG-12/24- [HCO3] ● If ratio of ΔAG/Δ[HCO3] is…. ○ >2 : metabolic alkalosis is present. ○ 1-2: no other metabolic disorder. ○ <1: additional non-anion gap metabolic acidosis
  • 98.
    Delta-delta made simple ●Step 1: calculate the ΔAG ● Step 2: add the ΔAG to the current [HCO3-] ● Step 3: compare this new [HCO3-] to the normal range of 22-28. ○ <22additional non-AG metabolic acidosis is present ○ >28additional metabolic ALKALOSIS is present. ○ 22-28: no additional metabolic disorder
  • 99.
  • 100.
    Answer  The patienthas high Ph- alkalemia  The pco2 is high(respiratory acidosis) and the bicarbonate is high  (metabolic alkalosis)  The high Ph and high bicarbonate tell us the metabolic alkalosis is the primary process  The AG-10,normal value  Summary:a primary metabolic alkalosis with respiratory compensation 04/01/2025 100
  • 101.
  • 102.
    Answer  The patienthas a low pH  The patient has a high pco2(respiratory acidosis) and a high bicarbonate (metabolic alkalosis).  The combination of low pH and high pco2 tells us that the respiratory acidosis is the primary process  Summary: primary respiratory acidosis with compensatory metabolic alkalosis 04/01/2025 102
  • 103.
  • 104.
    answer  The patienthas a very low pH(acidemia)  The patient has a low pcow(respiratory alkalosis) and a very low bicarbonate (metabolic acidosis).  The low pH in conjunction with the low bicarbonate tells us the metabolic acidosis is the primary process  The AG is elevated at 30- high AG MA  The respiratory alkalosis is the compensatory process,although despite a huge increase in Minute ventilation the patient still has a very low ph 04/01/2025 104
  • 105.
    Cont…  The deltagap is 30-12=18 and the delta delta is 18+2=20.  since the delta delta is below 22,we know that there is additional non gap metabolic acidosis as well  Summary: combined elevated anion gap and non gap metabolic acidosis with compensatory respiratory alkalosis 04/01/2025 105
  • 106.
  • 107.
    Answer  The patienthas a low pH(acidemia)  The pco2 is low ((respiratory alkalosis) and the bicarbonate is low(metabolic acidosis)  The combination of low pH and the low bicarbonate tells us that the metabolic acidosis is the primary process  The anion gap is elevated at 24.This tells us the patient has a primary high AG MA  The delta gap is 24-12=12. The delta delta is 12+17=29.because the Del- Del is greater than 26,we know the patient has a concurrent metabolic alkalosis  Summary: Primary elevated anion gap metabolic acidosis with respiratory compensation and a concurrent metabolic alkalosis 04/01/2025 107
  • 108.
    Case 3 ● 42year old man experienced crushing substernal chest pain and diaphoresis and shortness of breath and was brought to the emergency room. ○ Vital signs: BP 70/50 HR 110 RR 14 ○ Arterial blood gas analysis on room air: ○ pH 7.32/PCO2 24 mmHg/PO2 88 mm Hg/ HCO3ֿ 12 mEq/l /SaO2 96% ● Serum electrolytes: ○ Na 135 mEq/l K 5.4 mEq/l Cl 101 mEq/l , Lactate 12 mEq/l 04/01/2025 108
  • 109.
    Answer • Acidosis • Metabolicacidosis • Over-compensated • High anion gap • Delta/delta <1 • Respiratory alkalosis ans aditional non anaion gap acidosis • Primary high anion gap metabolic acidosis with secondary repiratory alkalosis and aditional non anion gap metabolic acidosis 04/01/2025 109
  • 110.
  • 111.

Editor's Notes

  • #3 Acidemia (as opposed to acidosis) is defined as a low arterial pH (<7.35), which can result from a metabolic acidosis, respiratory acidosis, or both
  • #9 Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ → H2PO4-), and ammonia to form ammonium (NH3 + H+ → NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load
  • #13 Acute rather than chronic hypocalcemia is seen in critically ill patients or as a consequence of certain medications and often does not require specific treatment. Transient hypocalcemia is seen with severe sepsis, burns, acute kidney injury, and extensive transfusions with citrated blood.
  • #16 Dilution acidosis — Dilution acidosis refers to a fall in serum bicarbonate concentration that is primarily due to rapid infusion of large volumes of normal saline, which contains neither bicarbonate nor the sodium salts of organic anions that can be metabolized to bicarbonate (such as lactate or acetate)
  • #17 The normal anion gap metabolic acidoses must, by definition, manifest relative hyperchloremia (a high chloride relative to the sodium concentration).
  • #18 The serum anion gap falls by approximately 2.5 mEq/L for every 1 g/dL (10 g/L) reduction below normal (4.5 g/dL) in the serum albumin concentration Thus, a serum potassium of 6 mEq/L will reduce the anion gap by 2 mEq/L. Marked hypercalcemia and/or hypermagnesemia can similarly reduce the anion gap. Another cause of a reduced or negative anion gap is immunoglobulin G (IgG) multiple myeloma
  • #20 D-lactic acidosis – D-lactic acid is generated by bacterial fermentation of ingested, but unabsorbed, carbohydrates. D-lactic acidosis results from excessive absorption of D-lactic acid from the lumen of the gastrointestinal tract, usually in patients with jejunoileal bypass or short bowel syndrome.
  • #21 When urine is exposed to gastrointestinal mucosa, which occurs after ureteral implantation into the sigmoid colon or the creation of replacement urinary bladder using a segment of the gastrointestinal tract Distal (type 1) RTA and type 4 RTA, in which tubular dysfunction is the primary problem and glomerular filtration is initially preserved
  • #23 In all simple acid-base disorders, the primary abnormality generates a compensatory response that results in both the HCO3 concentration and pCO2 moving in the same direction (either both will increase or both will decrease) This respiratory response to metabolic acidosis begins within 30 minutes and is complete by 12 to 24 hours.
  • #24 The pCO2 should approximate the decimal digits of the arterial pH. As an example, if the pH is 7.25, then the pCO2 should be approximately 25 mmHg
  • #25 This is consistent with a simple metabolic acidosis with appropriate respiratory compensation; all three of the compensation rules presented above are satisfied An inability to generate an appropriate hyperventilatory response is generally indicative of a significant underlying neurologic or respiratory disorder and represents a mixed acid-base disorder: metabolic acidosis and respiratory acidosis. Conversely, excessive hyperventilation, which reduces the pCO2 below the expected range, is indicative of mixed metabolic acidosis and respiratory alkalosis
  • #34 Similar considerations apply when hydrogen ions are retained because of impaired renal acid excretion due to distal (type 1) or type 4 RTA or hypoaldosteronism. In these conditions, a normal anion gap acidosis develops since there is no retention of unmeasured anions
  • #35 Severe and symptomatic acute acidemia can most rapidly be treated by the intravenous administration of sodium bicarbonate. Despite its potential adverse effects, sodium bicarbonate remains the most frequently used alkalinizing agent
  • #45 NRTI – inhibition of mitochondrial DNA polymerase Propylene glycol – solvent in lorazepam, diazepam, phenytoin Fructose competitively inhibits conversion of glycogen to glucose leading to lactic acidosis Isoniazid toxicity causes seizures and lactic acidosis
  • #49 CKD-Previously, sodium bicarbonate  therapy was not recommended. (fear of volume expansion and hypertension) Proximal RTA Administration of alkali result in increase urinary excretion of potassium Combination of sodium and potassium citrate should be administered.
  • #68 The ventilatory system is responsible for maintaining eucapnia by adjustment of alveolar minute ventilation (V ̇ A) to match the rate of CO2 production. An increase in arterial pCO2 can occur by one of three possible mechanisms: Presence of excess CO2 in the inspired gas Decreased alveolar ventilation Increased production of CO2 by the body
  • #80 This occurs when there is excessive loss of CO2 by hyperventilation of lungs.
  • #83 Acute hypocapnia causes cerebral vasoconstriction and decreases cerebral blood flow (in severe cases it can reach values less than 50% of normal) but flow essentially normalizes during sustained hypocapnia.
  • #86  Respiratory alkalosis itself is rarely life threatening. Therefore, emergent treatment is usually not indicated unless the pH level is greater than 7.5 If the PaCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may develop due to the renal compensatory drop in serum bicarbonate. respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the stimulus is controlled
  • #92 This is usually equal to 12 ± 4 meq/L and is usually due to the negatively charged plasma proteins as the charges of the other unmeasured cations and anions tend to balance out. When acid is added to the body, the [H+] increases and the [HCO3-] decreases. In addition, the concentration of the anion, which is associated with the acid, increases. This change in the anion concentration provides a convenient way to analyze and help determine the cause of a metabolic acidosis by calculating what is termed the anion gap.
  • #99 Explanation for the clinical picture: The patient has hypercalcemia and a metabolic alkalosis. In conjunction with a clinical history of heavy milk and calcium carbonate consumption, these abnormalities suggest the patient is suffering from milk-alkali syndrome. In response to metabolic alkaloses, patients develop hypoventilation. This explains his elevated PCO2and respiratory acidosis that, in turn, explains his hypoxemia
  • #100 Thepatienthashypercalcemiaandametabolicalkalosis.inconjuctionwithaclinicalhistoryofheavymilkandcalciumcarbonateconsumption,theseabnormalitiessuggestthepatientissufferingfrommilkalkalisyndrome.inresponsetometabolicalkaloses,patientsdevelophypoventilation,thisexplainselevatedpcoandrespiratoryacidosis
  • #101 Explanation for the clinical picture: The patient has very severe COPD and chronic carbon dioxide retention. As a result, you expect that at baseline, they will have a chronic respiratory acidosis (his baseline PCO2was 58) with a compensatory metabolic alkalosis. In this case, the clinical history suggests the patient is in an exacerbation. When the patient presents to the ER, his PCO2is elevated above his baseline. Because this is an acute change, the bicarbonate has not had time to adjust and the pH falls. This case is, therefore, an example of an respiratory acidosis
  • #103 Case 4 Explanation for the clinical picture: The patient has concurrent elevated anion gap and non-gap acidoses with respiratory compensation. The acidoses are so severe that, despite the high minute ventilation, the pH remains very low. This patient has a history of inhalant abuse and one of the commonly abused inhalants, toluene, can present with severe elevated anion gap acidosis with respiratory compensation. The severe elevated anion gap acidosis is due to accumulation of one of the main toluene metabolites, hippuric acid
  • #106 Explanation for the clinical picture: A history of epigastric pain, nausea and vomiting in conjunction with elevated lipase and amylase on laboratory studies is consistent with the diagnosis of pancreatitis. As a result of the pancreatitis, the patient has developed an elevated anion gap acidosis with respiratory compensation. The concurrent metabolic alkalosis is likely due to vomiting, which eads to hydrogen ion loss via the upper gastrointestinal tract.