Normal range PH
PH for acidosis
PH for alkalosis
Normal: 7.35-7.45
Acidosis: <7.35
Alkalosis: >7.45
Henderson-Hasselbach Equation
PH=6.1+log(HCO3/H2CO3)
(base/Acid)
PH=6.1+log(HCO3/0.03xCO2)
Normal blood gas values
CO2= 35-45 mmHg Remember 40
HCO3= 22-26mmHg Remember 24
O2= 95-100mmHg
SaO2= greater than or equal to 95%
Adverse consequences of acidosis
- 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
- CNS: coma or alter mental status
- Other: decreased respiratory muscle strength, Hypeventilation, and dyspnea
Adverse consequences of Alkalosis
- 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
- CNS: Decreased cerebral blood flow, seizures, lethargy, delirium, and stupor
- Other: decreased respiration (lungs try to hold on to the O2 they have)
How does our body generate acid?
- Diet: we eat about 1mEq/kg/day of acid
- Aerobic metabolism of glucose produces 15-20K mmol of CO2 each day
- Nonvolatile acids also formed: Lactic and pyruvic acid formed during anaerobic metabolism. Acetoacetic and beta-hydroxybutyric acid formed by triglyceride oxidation
what are the 3 ways the body regulates acid
- 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)
- Renal system regulation: Kidneys reabsorb bicarb in the proximal tubular and excrete H which created NEW bicarb in the distal tubular
- Ventilator regulation: The lungs: Chemoreceptors detect an increase in the CO2 and increase the rate and depth or ventilation to decrease CO2
Metabolic acidosis
Primary change and Compensation
Primary change: decreased HCO3 (kidneys aren’t absorbing/ generating enough HCO3)
Compensation: Decreased CO2 (lungs increase ventilation to blow off more CO2)
Metabolic Alkalosis
Primary change and Compensation
Primary change: Increased HCO3 Compensation: increased CO2 (lungs are breathing slower trying to hold onto the CO2)
Respiratory Acidosis
Primary change and Compensation
Primary change: increased CO2
Compensation: Increased HCO3 (kidneys are absorbing and generating more Bicarb)
Respiratory Alkalosis
Primary change and Compensation
Primarychange: Decreased CO2
Compensation: Decreased Bicarb (kidneys stop bicarb)
Metabolic acidosis what are the signs and first steps
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
Anion gap metabolic acidosis
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
- Ketoacidosis: increased acetoacetic acid and B-OH butyric acid
- Drug intoxications: aspirin very unique because it will cause metabolic acidosis and respiratory alkalosis
Pathophysiology of anion gap acidosis
MULEPAK
Methanol intoxication
Uremia
Lactic acidosis
Ethylene glycol
Paraldehyde ingestion
Aspirin
Ketoacidosis
Non-anion gap acidosis (hyperchloremic acidosis)
Loss of HCO3 replaced by Cl-
Causes
1.Gastrointestinal bicarbonate loss - diarrhea, pancreatic fistulas/biliary drainage
- Renal bicarbonate loss: TYPE II: proximal tubule has a decreased reabsorptive threshold Symptoms: Hyperaldosteronism, Hypokalemia, urine PH <5.3
- 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 - Acid and chloride administration
- Possibility that we give patient too much acid in TPN and cause acidosis
Symptoms of lactic acidosis - can lead to metabolic acidosis
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
Treatment of metabolic acidosis
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
Hazards of bicarbonate therapy
Overalkanization can reduce cerebral flow and can impair oxygen release for Hgb to tissue, Hypernatremia/hyperosmolality, CSF acidosis, Electrolyte shifts (Hypokalemia, Hypocalemia
Chronic bicarbonate therapy for metabolic acidosis
Average dose: 1-3mEq/kg/day
Metabolic alkalosis
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
Saline Responsive alkalosis (urinary chloride <10-20mEq/L)
Causes and treatment
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
Saline Resistant alkalosis causes and treatment
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
Respiratory acidosis
causes, symptoms and treatment
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
Respiratory alkalosis
Cause, symptoms, and treatment
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
