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Renal II Exam 3 > Acid Base Disorders > Flashcards

Acid Base Disorders Flashcards

1
Q

Acidemia vs. Acidosis

A

Acidemia is a decreased blood pH (normal is 7.36-7.44)

Acidosis is a clinical process in the body that decreases blood pH

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2
Q

Alkalemia vs. Alkalosis

A

Alkalemia is an increased blood pH (normal is 7.36-7.44)

Alkalosis a clinical process in the body that increases blood pH

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3
Q

Hyperkapnia and hypokapnia

A

Refers to increased or decreased pCO2 in the blood

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4
Q

Ventilation

A

Process by which inhaled air (including O2) reaches the alveoli of the lungs where gas exchange occur and exhaled air (including CO2) leaves the lungs

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5
Q

Minute Ventilation

A

Rate by which air reaches the alveoli.
Measured in Liters/minutes
Equal to Respiratory Rate (breaths per minute) x Tidal Volume (amount of air taken during one breath)

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6
Q

Hyperventilation vs. hypoventilation

A

Refers to increased or decreased minute ventilation rate respectively

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7
Q

Ventilation and pCO2

A

Hyperventilation leads to hypokapnia

Hypoventilation leads to hyperkapnia

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8
Q

Metabolic vs. Respiratory Acid-Base disorders

A

Respiratory acidosis and alkalosis are clinical processes that occur due to increase or decrease in ventilation and usually associated with pulmonary diseases
Metabolic acidosis and alkalosis are clinical processes that are not due to ventilation problems

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9
Q

Henderson-Hasselbach Equation

A

pH = 6.1 + log HCO3-/0.03 x pCO2

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10
Q

decreased pH and increased pCO2–> respiratory acidosis

A

hypoventilation–> hyperkapnia–>acidosis

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11
Q

increased pH and decreased pCO2-> respiratory alkalosis

A

hyperventilation–> hypokapnia–> alkalosis

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12
Q

decreased pH and decreased HCO3-

A 
Metabolic acidosis
Over-production or accumulation of acid
Loss of base (HCO3-)
Under-excretion of acid
All of the above will decrease HCO3 and will decrease pH
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13
Q

increased pH and increased HCO3-

A

Metabolic Alkalosis
Loss of acid
Under-excretion of base
Leads to increased HCO3 and increased pH

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14
Q

Primary vs. Secondary Acid-Base Disorders

A

Primary acid-base disorder results from a pathological process
Secondary acid-based “disorder” is a normal physiological compensation in response to a primary acid-base disorder

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15
Q

Compensation in Acid-Base Disorders- 3 types and the timing

A

Buffering—within minutes
Respiratory compensation (in metabolic disorders)—within hours
Metabolic compensation by kidneys — within 2-3 days

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16
Q

Acute vs. ChronicAcid-Base Disorders

A

Acute acid-base disorders results from the conditions that develop within hours of presentation
Chronic acid-base disorders are at least several days old
These terms are usually reserved to respiratory acid-base disorders
Acute respiratory disorders are uncompensated (resulting in acidemia or alkalemia).

Chronic respiratory disorders are fully compensated (pH is close to normal) and developed more than 2-3 days before presentation,
Sub-acute respiratory disorders are partially compensated (within 2 days frame)
Metabolic disorders could be fully or partially compensated depending on the degree of the acidosis and on a lung function

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17
Q

Simple vs. Mixed Acid-Base Disorders

A

Mixed disorders include combination of several acid-base disorders. They are very common
Metabolic acidosis and metabolic alkalosis
Respiratory acidosis and metabolic acidosis
Chronic respiratory acidosis and metabolic alkalosis
Etc.

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18
Q

Respiratory Acidosis

A

From hypoventilation
From decreased RR
- Decreased respiratory drive
—Drugs (Coma, Stroke

From decreased Tidal Volume

  • Neuro-muscular disorders
  • Severe kyphoscoliosis
  • Airways obstruction
  • COPD
  • Obstructive sleep apnea/Obesity
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19
Q

Anion Gap (A.G.)

A

A.G.=Na+– HCO3- - Cl-
Calculated from metabolic profile/electrolytes blood test
Represents unmeasured anions in the plasma
- Anionic proteins (albumin)
- Phosphate
- Sulfate
- Organic anions

20
Q

Causes of Acid-Base DisordersHigh AG Metabolic Acidosis

A 
Mnemonics is MUDPILES
Methanol
Uremia (End Stage Renal Disease)
Diabetic ketoacidosis
Paraldehyde
Infection, Iron, Isoniazide
Lactic acidosis
Ethylene glycol (antifreeze), alcohol
Salicylates, starvation ketoacidosis
21
Q

Uremic acidosis

A

Occurs when renal function is severely decreased (Creatinine clearance is less than 25ml/min)
Due to
- decreased excretion of acids
- decreased excretion of H+
- Decreased reabsorption/synthesis of HCO3
Accumulation of organic and inorganic anions
- Phosphates
- Sulfates

22
Q

Lactic Acidosis

A

Causes:
anaerobic metabolism in the tissues from Hypoxemia, Circulatory failure (hypotension, sepsis), Peripheral vessels blockage, Anemia,

Medications: Metformin, Some HIV meds, Isoniazide (toxic levels)

Liver failure due to decreased clearance
Thiamine deficiency
Hypophosphatemia
Sepsis (due to decreased perfusion of the tissues, impaired gluconeogenesis and poor clearance)
Seizures (due to release of lactate from muscles)- Short-lived [from overworking the muscles during the seizures]

Diagnosed by measuring level (venous or arterial)

23
Q

Diabetic Ketoacidosis

A

Insulin deficiency –> increased lypolysis –> increased fatty acid delivery to liver –> production of ketones –> acidosis
Associated with hyperglycemia
More often in Type I Diabetes Mellitus, but may happen in Type II as well
Usually part of the presentation of a new onset of type I DM
May be precipitated by patient’s non-compliance with insulin, infection (stress on the body), pancreatitis

24
Q

Alcoholic Ketoacidosis

A

Large ethanol intake–> ketones production
** No hyperglycemia
High osmolal gap–OG (normal is less than 10)
Difference between measured serum Osmolality and calculated serum osmolality
Calculated Osmolality = 2 (Na+) + (Glucose/18) + BUN/2.8
OG should be equal to Ethanol level/4.6
If OG more than that, look for other alcohols

25
Other alcohol poisoning: Ethylene glycol
``` Found in antifreeze and in industrial solvents Metabolites are highly toxic Increased OG Calcium Oxalate crystals in urine Acute Renal Failure is common ```
26
Other alcohol poisoning: methanol
Found in wood alcohol and windshield fluid Causes blindness and acute renal failure Increased OG
27
Salicylates poisoning
``` Usually a result of accidental or intentional overdose May cause metabolic acidosis and/or respiratory alkalosis Symptoms - Hemorrhage - Fever - nausea and vomiting, - Diaphoresis - Tinnitus - Pulmonary edema ```
28
Causes of Acid-Base Disorders- Normal AG Metabolic Acidosis
Diarrhea or Ileal drainage with stoma/bypasses - Due to loss of HCO3 - Except for Chloride wasting diarrhea with villous adenoma Decrease reabsorption of HCO3 by renal tubules (therefore increased loss) - Renal Tubular Acidosis - Due to diuretics ( carbonic anhydrase inhibitors [CAI]) Increase in anion intakes - Parenteral nutrition [sometimes we overdo the acids] Large amount of NaCl (expansion acidosis) - Due to dilution of the bicarbonate and to decreased renal bicarbonate reabsorption as a result of volume expansion
29
RTA Type I (Distal)
Decreased hydrogen ions excretion in the collecting ducts leading to alkaline urine and acidic serum Increased calcium excretion and decreased citric acid concentration leading to kidney stone formation Increased potassium loss leading to hypokalemia
30
RTA Type II (Proximal)
Defect in bicarbonate reabsorption in proximal tubules, so more bicarbonate is excreted, lowering serum bicarbonate and leading to acidemia and elevation in urine bicarbonate concentration. Increased Ca in the urine, but rarely leading to kidney stones due to normal citric acid concentration. Because distal tubules work OK, ability to acidify urine in response to acidemia is intact, so urine pH is low, and. High K loss also will lead to hypokalemia
31
RTA Type IV (distal hyperkalemic)
Occur in patient with moderate chronic renal failure Due to insufficient aldosterone production (hypo-reninemic) and/or aldosterone tubular resistance (due to renal failure) Insufficient K excretion leads to hyperkalemia
32
Urinary Anion Gap
To differentiate between renal and extrarenal HCO3 loss (RTA vs. diarrhea) Urine (Na++ K+) - Cl- Negative in extrarenal loss - Due to high level of unmeasured NH4+ - Excretion of NH4+ by healthy kidneys is a compensatory mechanism for acidosis Positive or non-existent in renal loss Due to low level of NH4+ and increased level of HCO3 What we calculate: Urine (Na++ K+) - Cl- What we actually mean: (HCO3- + Other anions) – (NH4+ + other cations) Extra-renal: increase NH4+, so gap is negative Renal: increase HCO3-, so gap is positive or 0
33
Causes of respiratory alkalosis
``` (from hyperventilation) Usually acute Pain Anxiety Salicylates overdose Fever Sepsis Hypoxia from some pulmonary disorders CHF Pneumonia PE Mild asthma Mechanical ventilation ```
34
Causes of metabolic alkalosis
Vomiting/NG suction - Due to lose of hydrochloric acid Contraction alkalosis due to increased HCO3- reabsorption - Dehydration - Diuresis (with diuretics other than CAI) Hypokalemia - Due to resulting increased mineralocorticoid secretion Recent correction of chronic respiratory acidosis - Due to recent metabolic compensation.
35
Clinical manifestations of metabolic acidosis
``` Kussmal respiration (sign of respiratory compensation) Nausea/vomiting Cardiac effects Arrhythmia Hypotension Neurological effects Confusion Lethargy Coma Symptoms of underlying disease ```
36
Clinical manifestations of respiratory acidosis
``` Ineffective respiration/respiratory distress Cardiac effects - Arrhythmia - Hypotension Neurological effects - Confusion - Lethargy - Coma (hypercapnic), CO2 narcosis Symptoms of underlying disease ```
37
clinical manifestation of metabolic alkalosis
``` Decreased respiration (compensatory). This may lead to ineffective respiration and hypoxia - Neurological - Parasthesia - Carpopedal spasm due to secondary hypocalcemia - Confusion - Seizures - Dizziness - Coma Weakness ```
38
Clinical manifestations of respiratory alkalosis
``` Hyperventilation Neurological - Parasthesia - Dizziness Symptoms of underlying disease ```
39
Important things to remember about ABG-- what is it used for?
Used predominantly for - Assessment of causes of dyspnea/hypoxia - Assessment of severity of pulmonary disease - Diagnosing respiratory failure - Managing patient on Ventilatory support Also used for diagnosing acid-base disorders
40
Basic Rules for interpreting ABG, clinical approach
- Determine the predominate process by assessing blood pH - Differentiate between primary and secondary (compensatory) acid-base disturbances - Remember: BODY NEVER OVER-COMPENSATES Remember main numbers: pH 7.40 pCO2 40 HCO3 24 - Determine if simple or mixed acid-base disorder presents - When math is about to fail you, pay attention to the clinical picture - Remember, you have a patient, not just the numbers.
41
Step-wise approach for acid-base problems
1. Look at pH: acidemia (7.4). 2. Look at HCO3- to determine if primary process is metabolic or respiratory. 3. Determine if process is compensated (chronic), uncompensated (acute), or partially compensated (somewhere in between) 4. Calculate anion gap to classify the metabolic acidosis or to determine if there is a mixed disorder with other types of acid-base disturbances 5. If anion gap is present, Calculate delta-delta gap to find mixed disorders 6. If metabolic disorder, look at pCO2 to determine if additional respiratory process exist. 7. Refer back to clinical picture and see if your calculations make any clinical sense
42
Steps 1 and 2 ``` ABG/chemistry results pH 7.02 (7.35-7.45) pCO2 20 (35-45) HCO3 7 (22-26) Na 122 (135-148) K 5.8 (3.5-5.2) Cl 88 (98-106) Glucose 798 (70-100) ```
Step 1. pH 7.02 acidemia predominant process is acidosis Step 2. Look at HCO3. If HCO3 follows pH, process is metabolic. If goes in the opposite direction, process is respiratory. Here HCO3 is down , and pH is down , so it’s a metabolic acidosis.
43
Step 3 ``` ABG/chemistry results pH 7.02 (7.35-7.45) pCO2 20 (35-45) HCO3 7 (22-26) Na 122 (135-148) K 5.8 (3.5-5.2) Cl 88 (98-106) Glucose 798 (70-100) ```
Determine if process is compensated or not. With metabolic disturbances, it’s easy. Look back at pH. If it’s normal, the process is compensated. If it’s abnormal, it’s uncompensated. In this case, it’s an uncompensated metabolic acidosis.
44
Step 4. Calculate Anion Gap ``` ABG/chemistry results pH 7.02 (7.35-7.45) pCO2 20 (35-45) HCO3 7 (22-26) Na 122 (135-148) K 5.8 (3.5-5.2) Cl 88 (98-106) Glucose 798 (70-100) ```
AG=Na-Cl-HCO3 First, have to correct Na for glucose . For each 100 mg/dl above 100, add 1. In this case , 122+ 798-100/100=129 AG: 129-88-7 = 34 (normal is 10) Assessment: High Anion Gap Metabolic Acidosis.
45
Step #5. Calculate Delta Anion Gap (D AG).
Delta AG = (AG – 10)/(24-HCO3) If D AG is 1-1.6, pure high AG metabolic acidosis If D AG is less than 1.0, concomitant non-AG acidosis If D AG is more than 1.6, concomitant metabolic alkalosis is present In our case – (34-10)/(24-7) = 1.4 Simple Non-compensated High AG Metabolic Acidosis
46
Step #6.
In case of metabolic disorders, look at pCO2. If changed in the opposite direction from HCO3, additional respiratory acid-base disorder of the same polarity as metabolic one exists. Here: pCO2 changed in the same direction, so no respiratory disorders
47
Step # 7.
Check back with clinical picture. This is a case of Diabetic Ketoacidosis One of the MUDPILES causes of high anion gap metabolic acidosis Why is not compensated? Acidosis is very severe. pCO2 is 20 (normal 40), so partial compensation is present but not sufficient because of the degree of the acidosis

Renal II Exam 3 (15 decks)

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