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PHRM 864 - EXAM 3 > Acid Base > Flashcards

Acid Base Flashcards

1
Q

Normal range PH

PH for acidosis
PH for alkalosis

A

Normal: 7.35-7.45

Acidosis: <7.35
Alkalosis: >7.45

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2
Q

Henderson-Hasselbach Equation

A

PH=6.1+log(HCO3/H2CO3)
(base/Acid)

PH=6.1+log(HCO3/0.03xCO2)

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3
Q

Normal blood gas values

A

CO2= 35-45 mmHg Remember 40

HCO3= 22-26mmHg Remember 24

O2= 95-100mmHg

SaO2= greater than or equal to 95%

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4
Q

Adverse consequences of acidosis

A
  1. Cardiovascular: acidosis causes impairment of cardiac contractility and increased pulmonary vascular resistance and arrhythmia which lead to decreased cardiac output

2.Metabolic: insulin resistance, inhibition of anaerobic glycolysis, hyperkalemia

  1. CNS: coma or alter mental status
  2. Other: decreased respiratory muscle strength, Hypeventilation, and dyspnea
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5
Q

Adverse consequences of Alkalosis

A
  1. Cardiovascular: arteriolar constriction leads to decreased coronary blood flow which leads to decreased anginal threshold. Arrhythmias due to hypokalemia

2.Metabolic: Decrease K, Ca, and Mg
Stimulation of anaerobic glycolysis which increases risk of heart disease due to ATP

  1. CNS: Decreased cerebral blood flow, seizures, lethargy, delirium, and stupor
  2. Other: decreased respiration (lungs try to hold on to the O2 they have)
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6
Q

How does our body generate acid?

A
  1. Diet: we eat about 1mEq/kg/day of acid
  2. Aerobic metabolism of glucose produces 15-20K mmol of CO2 each day
  3. Nonvolatile acids also formed: Lactic and pyruvic acid formed during anaerobic metabolism. Acetoacetic and beta-hydroxybutyric acid formed by triglyceride oxidation
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7
Q

what are the 3 ways the body regulates acid

A
  1. Buffering: Fist line of defense and include bicarbonate/carbonic acid (acidity can be controlled by bicarb or CO2 due to kidneys excreting and lungs retaining when needed), Phosphates (Inorganic is limited extracellularly and organic limited intracellularly - more useful), and protein (albumin/ hemoglobin are more effective intracellular buffers vs extracellular)
  2. Renal system regulation: Kidneys reabsorb bicarb in the proximal tubular and excrete H which created NEW bicarb in the distal tubular
  3. Ventilator regulation: The lungs: Chemoreceptors detect an increase in the CO2 and increase the rate and depth or ventilation to decrease CO2
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8
Q

Metabolic acidosis

Primary change and Compensation

A

Primary change: decreased HCO3 (kidneys aren’t absorbing/ generating enough HCO3)

Compensation: Decreased CO2 (lungs increase ventilation to blow off more CO2)

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9
Q

Metabolic Alkalosis

Primary change and Compensation

A

Primary change: Increased HCO3 Compensation: increased CO2 (lungs are breathing slower trying to hold onto the CO2)

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10
Q

Respiratory Acidosis
Primary change and Compensation

A

Primary change: increased CO2

Compensation: Increased HCO3 (kidneys are absorbing and generating more Bicarb)

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11
Q

Respiratory Alkalosis
Primary change and Compensation

A

Primarychange: Decreased CO2

Compensation: Decreased Bicarb (kidneys stop bicarb)

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12
Q

Metabolic acidosis what are the signs and first steps

A

Low PH <7.35 and low bicarb levels HCO3 <24 and due to compensation mechanism of lungs CO2 decreased <40

  • want to calculate the anion gap immediately
  • Anion gap = NA - (Cl + HCO3)
  • Normal anion gab is 3-11mEq/L
  • If patient has a gap over 11 its anion gap metabolic acidosis
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13
Q

Anion gap metabolic acidosis

A

Low PH <7.35 and low bicarb levels HCO3 <24 and due to compensation mechanism of lungs CO2 decreased <40 and anion gap >11

Want to calculate the delta
take the (patients anion gap -10) and add it to their bicarb level if it is elevated (above normal range of bicarb levels >26) it tells us that patient is having mixed disorder

Causes of anion gap metabolic acidosis
1. Lactic acidosis: elevated levels of lactate are due to decreased clearance from the livers (also little bit of disposal in kidney, muscle and CNS but mainly liver) -can be seen in patients with shock, seizures, Leukemia, Hepatic/renal failure, diabetes mellitus, and malnutrition

  1. Ketoacidosis: increased acetoacetic acid and B-OH butyric acid
  2. Drug intoxications: aspirin very unique because it will cause metabolic acidosis and respiratory alkalosis
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14
Q

Pathophysiology of anion gap acidosis
MULEPAK

A

Methanol intoxication
Uremia
Lactic acidosis
Ethylene glycol
Paraldehyde ingestion
Aspirin
Ketoacidosis

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15
Q

Non-anion gap acidosis (hyperchloremic acidosis)

A

Loss of HCO3 replaced by Cl-

Causes
1.Gastrointestinal bicarbonate loss - diarrhea, pancreatic fistulas/biliary drainage

  1. Renal bicarbonate loss: TYPE II: proximal tubule has a decreased reabsorptive threshold Symptoms: Hyperaldosteronism, Hypokalemia, urine PH <5.3
  2. Reduced renal H excretion:
    -Type I RTA: Hypokalemia causes: Damage to the distal tubule, because H excretion is reduced there isnt enough to do an ion exchange with sodium so potassium takes part of this ion exchange and we see an increased excretion of potassium symptoms: Hypokalemia, urine PH> 5.3
    -Type IV RTA: Aldosterone stimulates H excretion so with less aldosterone we hold on to potassium which causes hyperkalemia which further causes the body to hold onto H and lead to acidosis
  3. Acid and chloride administration
    - Possibility that we give patient too much acid in TPN and cause acidosis
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16
Q

Symptoms of lactic acidosis - can lead to metabolic acidosis

A

Kussmaul respiration (breathing fast and deep - lungs trying to blow of CO2)
Peripheral vasodilation causing flushing and tachycardia, Hyperkalemia, Lethargy/coma, Nausea/vomiting, Bone demineralization in chronic acidotic states

17
Q

Treatment of metabolic acidosis

A

Acute bicarbonate therapy for severe and acute bicarb loss
consider for use if pH <7.10-7.15, good indications for use: hyperkalemia, pH<7.10, cardiac arrest after defibrillation, bentilation, and medications have been utilized, and overdose (depending on what drug pt is overdosing on)

Dosing 0.5L/kg(IBW) x (desired HCO3 - actual HCO3)
use 12 mEq/L for desired HCO3
Give 1/3 to 1/2 the calculated dose and monitor ABG

IF patient is in cardiac arrest give 1mEq/kg

18
Q

Hazards of bicarbonate therapy

A

Overalkanization can reduce cerebral flow and can impair oxygen release for Hgb to tissue, Hypernatremia/hyperosmolality, CSF acidosis, Electrolyte shifts (Hypokalemia, Hypocalemia

19
Q

Chronic bicarbonate therapy for metabolic acidosis

A

Average dose: 1-3mEq/kg/day

20
Q

Metabolic alkalosis

A

Characterized by increased PH >7.45, increased HCO3 >30mEq/L and a compensatory hypoventilation resulting in increased CO2

Causes: loss of acid from GI tract or urine, Administration of HCO3 or a bicarbonate precursor, contraction alkalosis (loss of Cl rich fluid and HCO3 poor fluid, could also be impairment in renal HCO3 excretion

Often volume and chloride depletion contribute: decrease in atrial blood volume, decreased ability of kidney to excrete HCO3, with volume depletion, capacity of the proximal tubule to reabsorb HCO3 increases

21
Q

Saline Responsive alkalosis (urinary chloride <10-20mEq/L)

Causes and treatment

A

urinary chloride <10-20mEq/L
1. Diuretics
2. Vomiting and NG suction
3. exogenous HCO3 administration of blood transfusion

Treatment:
-fluid/electrolyte replacement
Potassium supplementation if needed
- Carbonic anhydrase inhibitors for patients who cannot tolerate fluid - HCl acid fluid if pH >7.55
- Can do adjunct therapy like PPIs or H2 for patients vomititng to prevent ulcers

Monitoring I/O, BP, HR, Lung sounds, electrolytes, and edema

22
Q

Saline Resistant alkalosis causes and treatment

A

Urinary chloride >20mEq/L
NO CHLORIDE depletion seen here
1. Increased mineralcorticoid activity
2. Hypokalemia: increases H secretion and increases HCO3 reabsoprtion
3. Renal tubular chloride wasting: impaired NaCl reabsorption

Treatment:
-Correct the underlying cause
-correct hypokalemia with potassium sparing diuretic or KCl supplementation
- add spironolactone
- correct hyperaldosteronism
Monitoring I/O, BP, HR, Lung sounds, electrolytes, and edema

23
Q

Respiratory acidosis
causes, symptoms and treatment

A

Low PH increased CO2 and increased HCO3
Causes:
1.Airway obstructions: asthma, choking, aspiration (lungs cant breath off the CO2)
2. Reduced stimulus for respiration from CNS: Drug overdose, sleep apnea, CNS infections, trauma
3. Failure of heart or lungs: PE, Cardiac arrest
4. Neuromuscular defects affecting nerves (ALS, Guillain-Barre)
5. Mechanical ventilation

Symptoms: SOB/Dyspnea, HA, drowsiness, confusion, coma, seizure, Tachycardia, arryhtmias, and/or hypotension

Treatment:
Correct underlying cause
Mechanical ventilation or oxygen (caution with oxygen in COPD patients dont want to go too hard or you can kill them)

In some cases we will use bicarbonate with acute acidosis if pH<7.5 where patient is at greater risk for arrhythmia’s

24
Q

Respiratory alkalosis
Cause, symptoms, and treatment

A

Increased pH >7.45, decreased CO2 <40 and decreased HCO3 <24

Causes:
1. Central stimulation of respiration:anxiety, trauma, injury, or pain
2. Peripheral stimulation of respiration: hypotention, high altitude, hypoxemia, CHF
3. Mechanical ventilation
4.Pulmonary: edema, PE, pneumonia
5. Salicylate intoxication (causes metabolic acidosis and respiratory alkalosis

Symptoms:
Lightheadedness, confusion, seizures, decreased cerebral blood flow, tetany/muscle cramps, N/V

Treatment:
Treat the underlying cause
ventilation, sedation, paralysis

25
Q

Determine the type of disorder, possible causes, and possible treatment

7.32/31/90/15/98%
Na: 137 K: 4.9 Cl 115 HCO3: 15
Pt. receiving TPN

A

ph is 7.32 low
CO2 is 31 (9 below)
HCO3 is 15 (9 below)
Anion gap= 137 - (115+15) = 7

Non-anion gap metabolic acidosis
- could be due to patients TPN would want to assess formula and change

26
Q

Determine the type of disorder, possible causes, and possible treatment

7.23/27/87/11/97%
Na: 138 K: 5.6 Cl 108 HCO3: 12 Glu:400
RR 25

A

7.23 low
CO2 is 27 (13 below)
HCO3 is 11 (13 below)
Metabolic acidosis
anion gap=138-(108+12) = 18 elevated
18-10=8 8+12= 20 - not elevated so its not a mixed disorder

  • patient is experiencing anion gap metabolic acidosis
  • could be any of MULEPAK but from what we have about this specific patient most likely ketoacidosis as the patients glucose is 400
27
Q

Determine the type of disorder, possible causes, and possible treatment

7.0/28/208/10/99.1%
Na: 141 K: 3.9 Cl 108 HCO3: 12
BP 70/40 Pt. in shock
Ht 5’9 wt: 80kg

A

Low ph
CO2 low (12 below)
HCO3 low (14 below)
Metabolic acidosis
anion=141-(108+12)=21
21-10=11 11+12=21 delta not elevated not mixed
anion gap metabolic acidosis
since patient is in shock high chance acidosis is due to lactic acidosis
patients Ph is <7.1 so we could give bicarb
0.5mg x IBW x (12- bicarb level) = 70.7 –> want to split this dose by half or 1/3 for initial dosing
IBW = 50 + 2.3(9)= 70.7

28
Q

Determine the type of disorder, possible causes, and possible treatment

7.22/72/29/28/48.1%

BP 95/60 HR 92 RR 6

A

pH low - 7.22
CO2 high (32 increase)
HCO3 high (4 increase)
Is it acute or chronic?
32 x 0.1 = 3.2 - acute respiratory acidosis

causes could be asthma, chocking, overdose, aspiration

treatment would be to fix the underlying cause

29
Q

Metabolic acidosis
how to know if patient compensated fully

A

take bicarb level x 1.25

if the CO2 level has decreased by that number or more then full compensation

30
Q

Causes of anion gap metabolic acidosis

A

Methanol intoxication
Uremia
Lactic acidosis
Ethylene glycol
Paraldehyde ingestion
Aspirin
Ketoacidosis

PHRM 864 - EXAM 3 (6 decks)

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