abg seminar for pna cebu

Acid-base disorders and its implications: Therapy in a Nursing

Perspective(July 23, 2014)

EMILIANO IAN B. SUSON II, ED.D, USRN, MAN, RN

“SIR EYE”

Objectives

Describe physiology involved in acid base balance of the body

Review causes and treatments of acid base disorders

Identify normal arterial blood gas values

Interpret results of ABG samples

Interpret oxygenation state of a patient using reported ABG values

2

Interpretation of ABG

» Very important for health care providers

» Usefulness of this tool depends on being able to interpret correctly the results

» Critically ill patients

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Acid base disorders

12000 to 15000 mEq of volatile acids are produced daily by body and excreted as CO2 by lungs

1 mEq / kg / day of non-volatile acids (sulfuric and phosphoric acids) are produced daily by body and excreted by the kidneys

The most important buffers in the body are, hemoglobin, plasma proteins and bicarbonate

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Acid base disorders

SIMPLE ACID BASE DISORDER: when there is only one primary disorder

MIXED ACID BASE DISORDER: when there are two or more primary disorders present at the same time

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Normal values

pH 7.35-7.45 7.40

PaCO2 35-45 mmHg 40

PaO2 70-100 mmHg

HCO3- 24±2 24

Met-Hb <2%

CO-Hb <3%

BE -2 to 2 mEq/L

CaO2 16-22 ml/dL

A gap 10±2 12

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7

8

9

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Buffers

1. Protein Buffer Systems

Amino Acid buffers

Hemoglobin buffers

Plasma Protein buffers

2. Phosphate Buffer Systems

3. Carbonic Acid – Bicarbonate Buffer System

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12Bicarbonate buffer

Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)

Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 ↔ H2CO3 + NaCl

NaOH + H2CO3 ↔ NaHCO3 + H2O

13Phosphate buffer

Major intracellular buffer

H+ + HPO42- ↔ H2PO4-

OH- + H2PO4- ↔ H2O + H2PO4

2-

14Protein Buffers Includes hemoglobin, work in blood and ISF

Carboxyl group gives up H+

Amino Group accepts H+

Side chains that can buffer H+ are present on 27 amino acids.

The 10 essential amino acids are:(PVTMATHILL)

Phenylalanine, Valine, Tryptophan, Methionine, Arginine,

Threonine, Histidine, Isoleucine, Leucine, Lysine

10 Amino acids the body produces:

alanine, asparagine, aspartic acid, cysteine, glutamic acid, glutamine, glycine, proline, serine and tyrosine

152. Respiratory mechanisms

Exhalation of carbon dioxide

Powerful, but only works with volatile acids

Doesn’t affect fixed acids like lactic acid

CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-

Body pH can be adjusted by changing rate and depth of breathing

163. Kidney excretion

Can eliminate large amounts of acid

Can also excrete base

Can conserve and produce bicarb ions

Most effective regulator of pH

If kidneys fail, pH balance fails

17Rates of correction

Buffers function almost instantaneously

Respiratory mechanisms take several minutes to hours

Renal mechanisms may take several hours to days

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19

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21Acidosis Principal effect of acidosis is depression of the CNS through ↓ in synaptic

transmission.

Generalized weakness

Deranged CNS function the greatest threat

Severe acidosis causes

Disorientation, Coma, Death

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Alkalosis

Alkalosis causes over excitability of the centraland peripheral nervous systems.

Numbness

Lightheadedness

It can cause : Nervousness

muscle spasms or tetany

Convulsions

Loss of consciousness

Death

23Respiratory Acidosis

Acute conditons:

Adult Respiratory Distress Syndrome

Pulmonary edema

Pneumothorax

24Compensation for Respiratory Acidosis

Kidneys eliminate hydrogen ion and retain bicarbonate ion

25Signs and Symptoms of Respiratory Acidosis

Breathlessness

Restlessness

Lethargy and disorientation

Tremors, convulsions, coma

Respiratory rate rapid, then gradually depressed

Skin warm and flushed due to vasodilation caused by excess CO2

26Treatment of Respiratory Acidosis

Restore ventilation

IV lactate solution

Treat underlying dysfunction or disease

27Respiratory Alkalosis

Conditions that stimulate respiratory center:

Oxygen deficiency at high altitudes

Pulmonary disease and Congestive heart failure – caused by hypoxia

Acute anxiety

Fever, anemia

Early salicylate intoxication

Cirrhosis

Gram-negative sepsis

28Compensation of Respiratory Alkalosis

Kidneys conserve hydrogen ion

Excrete bicarbonate ion

29Treatment of Respiratory Alkalosis

Treat underlying cause

Breathe into a paper bag

IV Chloride containing solution – Cl- ions replace lost bicarbonate ions

30Metabolic Acidosis

Bicarbonate deficit - blood concentrations of bicarb drop below 22mEq/L

Causes:

Loss of bicarbonate through diarrhea or renal dysfunction

Accumulation of acids (lactic acid or ketones)

Failure of kidneys to excrete H+

31Symptoms of Metabolic Acidosis

Headache, lethargy

Nausea, vomiting, diarrhea

Coma

Death

32Compensation for Metabolic Acidosis

Increased ventilation

Renal excretion of hydrogen ions if possible

K+ exchanges with excess H+ in ECF

( H+ into cells, K+ out of cells)

33Treatment of Metabolic Acidosis

IV lactate solution

34Metabolic Alkalosis Bicarbonate excess - concentration in blood is greater than

26 mEq/L

Causes:

Excess vomiting = loss of stomach acid Excessive use of alkaline drugs

Certain diuretics Endocrine disorders

Heavy ingestion of antacids

Severe dehydration

35Symptoms of Metabolic Alkalosis

Respiration slow and shallow

Hyperactive reflexes ; tetany

Often related to depletion of electrolytes

Atrial tachycardia

Dysrhythmias

36Treatment of Metabolic Alkalosis

Electrolytes to replace those lost

IV chloride containing solution

Treat underlying disorder

37Example

A patient is in intensive care because he suffered a severe myocardial infarction 3 days ago. The lab reports the following values from an arterial blood sample:

pH 7.3

HCO3- = 20 mEq / L ( 22 - 26)

pCO2 = 32 mm Hg (35 - 45)

38Diagnosis

Metabolic acidosis

With compensation

Acid base disordersMETABOLIC ACIDOSIS: HCO3 <24 OR Anion Gap

>12

METABOLIC ALKALOSIS: HCO3 >24

RESPIRATORY ALKALOSIS: PCO2 <40 or PCO2 less than expected for primary metabolic abnormality

RESPIRATORY ACIDOSIS: PCO2 >40 or PCO2 higher than expected for primary metabolic abnormality

HIGH ANION GAP (>12-20) always indicates primary metabolic acidosis

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Acid base disorders and compensatory response

pH HCO3- PaCO2

Metabolic acidosis

Metabolic alkalosis

Respiratory acidosis

Respiratory alkalosisCompensatory response never brings the pH back to normal if the pH is in acidic direction, it tells you that the process or processes in acidic direction are the primary disorders

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Anion Gap

Na-(Cl+HCO3)= 12±2

Estimates unmeasured anions

Normal is 12

Hypoalbuminemia:

Correct anion gap: 2.5 per gram of albumin below 4

Calculate osmolal gap if anion gap is elevated

OSM gap = measured OSM-2(Na)-glu/18-BUN/2.8 = <10

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Urinary anion gap

Useful in differential diagnosis of non gap acidosis

U anion gap= Na + K – Cl

A negative U. Anion Gap ie Cl >> Na + K suggests appropriate urinary NH4 excretion and G.I. loss of HCO3

A positive U. Anion Gap ie. Cl << Na + K suggests RTA with distal acidification defect and inadequate NH4 excretion in urine

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Acidosis (Low pH)

Lowering extracellular pH by rising concentration of hydrogen ions

Fall in bicarbonate concentration

Elevation in PCO2

Decreases force of cardiac contractions

Decreases vascular response to catecholamines

Decreases response of certain medications

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Alkalosis (High pH)

Elevation of the pH of the extra cellular fluid

Lowering hydrogen ion concentration

Elevation in plasma bicarbonate

Reduction in PCO2

Impairs oxygenation

Impairs muscular function

Impairs neurological function

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Metabolic acidosis

Anion Gap

Methanol

Uremia

DKA

Paraldehyde

INH

Lactic acidosis

Ethylene glycol

Salicylate

Non Gap

Hyperalimentation

Acetazolamide

Renal tubular acidosis

Diarrhea

Ureterosigmoidostomy

Pancreatic fistula

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Metabolic alkalosis

Gain of bicarbonate by abnormal renal absorption

Volume contraction (low urine chloride)

Vomiting: loss of H+

Diuretics: depletion ECF

Severe hypokalemia

Renal failure

Mineralocorticoid excess (high urine chloride)

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At a Glance Acid- Base Disorders

Acid-base

disorder

Causes Signs and

Symptoms

Respiratory

acidosis

Hypoventilation,

Neuromuscular

disorders, Airway

obstruction, CNS

depression

↑PR, ↑RR, ↑BP,

Mental

cloudiness,

Feeling of

fullness in the

Head, ↑ICP

Ventricular

Fibrillation, Papilledema,

Dilated

Conjunctival

Blood vessel,

Hyperkalemia,

Tachypnea,

Cyanosis

Acid-base

disorder

Causes Signs and

Symptoms

Respiratory

alkalosis

Hyperventilation,

Sepsis,

Pregnancy,

Mechanical

Ventilation, fever

Lightheadedness

Inability to

Concentrate,

Numbness and

Tingling, Tinnitus

Loss of

consciousness

At a Glance Acid- Base Disorders

Acid-base

disorder

Causes Signs and

Symptoms

Metabolic

acidosis

Diabetic

Ketoacidosis,

Renal failure

Methanol/aspirin

Overdose,

Renal tubular

Acidosis,

Diarrhea, Chronic

alcoholism

Headache, ↓ BP

Confusion

Drowsiness

↑ RR and depth

Nausea, Vomiting

↓Cardiac output

Cold and clammy

Skin, Shock,

Dysrhythmias

At a Glance Acid- Base Disorders

Acid-base

disorder

Causes Signs and

Symptoms

Metabolic

alkalosis

vomiting

diuretics

alkali ingestion

Tingling of fingers

and toes, Dizziness,

Hypertonic muscles,

Symptoms of

Hypocalcemia, ↓ RR,

Atrial tachycardia

Hypokalemia, Paralytic

Ileus, Dysrhythmia

At a Glance Acid- Base Disorders

Acid-Base Imbalances Management

TYPE OF

IMBALANCE

MANAGEMENT

Respiratory

Acidosis

- Improving ventilation

- Bronchodilators

- Antibiotics for infection

- Thrombolytics & anticoagulants

(pulmonary emboli)

- Pulmonary hygiene

- Mechanical ventilation

- Semi-Fowler’s position

Acid-Base Imbalances Management

TYPE OF

IMBALANCE

MANAGEMENT

Respiratory

Alkalosis

- Treatment of the underlying

cause

- Breathe into a paper bag

- Sedative

Acid-Base Imbalances Management

TYPE OF

IMBALANCE

MANAGEMENT

Metabolic

Acidosis

- Treatment is correcting the

underlying defect.

- Eliminating source of chloride

- Bicarbonate

- Alkalizing agents

- Hemodialysis

- Peritoneal dialysis

Acid-Base Imbalances Management

TYPE OF

IMBALANCE

MANAGEMENT

Metabolic

Alkalosis

- Treatment of underlying

disorder

- Chloride supply

- Sodium chloride fluids

- KCl

- H2-receptor antagonists

(Cimitidine)

- Carbonic anhydrase inhibitors

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Cases

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HEMOGLOBIN

PLT

WBC

HEMATOCRIT

SEGMENTERS

RBC

pH K

Na

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12-14

140k-440k

5k-10k

38-42

SEGMENTERS

4-8

7.35-7.45 4.0-5.1

135-145

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Hemoglobin – this is the part of your red blood cell which carries

oxygen all over the body. If your hemoglobin levels are decreased it

could pertain to anemia, bleeding, patients with chronic kidney

disease, or a possible blood dyscrasia. If your hemoglobin levels

are elevated we could consider polycythemia vera and dehydration.

Red Blood Cell (RBC) – this part of the CBC tells you the number

of cells that could carry oxygen in the body. Same with hemoglobin,

decrease levels of RBC could also be secondary to anemia or

bleeding and increase levels could also be secondary to

polycythemia or dehydration.

Hematocrit – this measures the amount of space in the blood

being occupied by your red blood cells. Causes for the increased

and decreased of hematocrit are the same with your hemoglobin

and red blood cells.

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White Blood Cell (WBC) – this are the cells in the body that fight

off invaders like infections. An increase or decrease in WBC count

could represent an ongoing infection or a malignancy like your

leukemia. Also included in the CBC is the 5 differential count for

your WBC, namely:

Neutrophils or segmenters – this type of WBC are the primary

cells that respond to a bacterial infection. High levels of your

neutrophils usually represent and ongoing infection, an

inflammation, malignancy, cause by some drugs, etc. Low levels of

your neutrophils could be seen in patients with viral infection,

autoimmune diseases, some medications and malignancy.

Lymphocytes – this type of WBC represent 20-40% of your

circulating WBC in the blood. An increased in lymphocyte count

usually represents an acute infection especially viral infections,

leukemia, smoking, etc. Low lymphocyte count is usually not

significant.

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Monocytes – this comprises 3-8% of all white blood cells in the

body. An increase in monocyte could signify a chronic infection like

your tuberculosis or a chronic inflammation condition like your

inflammatory bowel disease and malignancy. Low levels of

monocytes are usually none significant if other cells are normal.

Basophils – this comprises only 0.01-0.3% of all white blood cells

in the blood. This type could produce histamine. Increased

numbers could represent a myeloproliferative disorder.

Eosinophils – comprises 1 – 6% of all white blood cells in the

blood stream. They are usually increase in cases of allergy, asthma

and in parasitic infections. Low levels are usually not significant.

Platelet Count – the normal platelet count ranges from 150,000 –

400,000 /L and this cell is involved in the clotting cascade of the

body. Low levels of this cell could cause easy bruising and

bleeding. Causes of low platelet count include infections (ex:

dengue fever), autoimmune disease, liver disease, idiopathic

thrombocytopenic purpura, etc.

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Red Cell Indices – this are investigated when considering

diseases like your thalassemia or sickle cell anemia.

MCV (mean corpuscle volume) – telling you the average size of

the red blood cell (80-100)

MCH (mean corpuscle hemoglobin) – shows the average

amount of hemoglobin in each red blood cell (26-34)

MCHC (mean corpuscle hemoglobin concentration) – average

amount of hemoglobin in the red blood cell compared to their

average size. (31-37)

RDW – (11.5 -14.5)

ABG SHORTCUT

Laboratory studies

ABG: pH/PaCO2/PaO2/HCO3/O2sat

ABG: 7.38-7.44/35-45/80-100/22-26/95-100

What is the acid base disturbance and what is the cause

Na135-145

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K3.5-5.1

AG7-16

CO222-30

BUN5-25

Crea0.6-1.2

Glu70-110

Ca8.5-10.1

Cl98-107

CHEMICAL COMPOSITIONS OF BODY FLUIDS

Extracellular Fluid Intracellular Fluid

Na+ 142 mEq/L 10mEq/L

K+ 4mEq/L 140 mEq/L

Ca2+ 2.4 mEq/L 0.0001 mEq/L

Mg2+ 1.2 mEq/L 58 mEq/L

Cl- 103 mEq/L 4 mEq/L

HCO3- 28 mEq/L 10 mEq/L

Phosphates 4 mEq/L 75 mEq/L

SO42- 1 mEq/L 2 mEq/L

Glucose 90 mg/dl 0-20 mg/dl

Amino Acids 30 mg/dl 200 mg/dl

CHEMICAL COMPOSITIONS OF BODY FLUIDS

Extracellular Fluid Intracellular Fluid

Cholesterol 0.5 g/dl 2-95 g/dl

Phospholipids 0.5 g/dl 2-95 g/dl

Neutral fat 0.5 g/dl 2-95 g/dl

PO2 35 mm Hg 20 mm Hg

PCO2 46 mm Hg 50 mm Hg

pH 7.4 7.0

Proteins 2 g/dl 16 g/dl

5 mEq/L 40 mEq/L

Arterial Blood Sampling

NURSE PHLEBOTOMIST

Indications

To assess.

Respiratory Status

Assess oxygenation and ventilation

Acid Base Balance

Phlebotomy. Used if venous route is unavailable or inaccessible due to trauma or burns. Usually a femoral puncture, uncommon variation.

Contraindications

Overlying infection or burn at insertion site.

Absent collateral circulation.

Arteriovenous shunt. Often radial or brachial.

Severe atherosclerosis

Raynauds disease.

Coagulopathy.

Sites

Preferred radial or femoral arteries.

Less common. Dorsalis pedis and posterior tibial.

Avoid. Branches without collateral supply. Example is the brachial artery.

Complications

Bleeding causing hematoma.

Arterial occlusion causing thrombus or dissection.

Infection causing arteritis or cellulitis.

Embolization

Last 3 uncommon.

Normal Values

pH, 7.36 to 7.44. For acid base status of blood.

pCO2, 38 to 44 mmHg. Reflects ventillation.

pO2, 85 to 95 mmHg. Reflects oxygenation.

HCO3, 21 to 27 meq per litre. Key blood buffer.

Base excess, plus or minus 2 meq per litre

ABG quiz. http://www.vectors.cx/med/apps/abg.cgi

Pathophysiology

Metabolic alkalosis

Metabolic acidosis

Respiratory alkalosis

Respiratory acidosis

Initial Preparation

Wash hands

Gloves

Protective eye wear

Iodine swab. Povidone-iodine, betadine. Followed by alcohol swab

Arterial blood gas sampling kit

2 x 2 cm gauze

Bag of ice. To store sample

Allens Test

Indicates collateral circulation to hand.

Radial artery on non dominant hand.

Palpate radial artery.

Simultaneouslys palpate ulnar artery, or as close to that area as possible.

Patient makes a fist. Palpate both arteries for10 seconds.

Release ulnar artery and witness blood flow and pinking of the hand via collateral radial artery

Radial artery is now a candidate for testing.

Set Up

Patient seated on stretcher

Rolled up towel under wrist. That hyperextends wrist, bringing artery closer to surface.

Clean area in a cicular motion with iodine. Allow to dry.

Wipe away iodine with alcohol. While drying, open sampling kit.

Sampling Kit

3 pieces

1. Orange air ball or cube. Used to expel excess air from the syringe.

2. Black cap for syringe, used for transport.

3. 3 cc, cubic centimetres heparinised syringe. With needle attached.

Sampling Kit Use

Pull back slightly on plunger, so once needle is in artery, natural pulsations will fill the syringe.

Remove clear needle cap. Locate the bevel. Bevel is a slanted opening on one side of the needle tip. We want bevel facing upward, so you can see it.

Syringe Use

45 degrees, sharper angle.

Hold like a dart or pen.

Feeling pulse under non syringe finger is the only landmark for orientation.

Before piercing skin, roll finger back slightly from artery, so you dont stab yourself in the finger.

Flash of blood into hub of needle. Artery has been accessed.

Blood will pulse into syringe. 1.5 to 2.0 cc required.

Cover needle with gauze. Quickly remove needle.

After Care

Physician applies pressure to gauze for 5 minutes. 10 minutes if patient is on anticoaggulant therapy.

Optional to ask patient to do this instead.

Blood Care

Insert needle into orange air cube or ball. Want bevel covered, dont want needle to go through cube.

Push down on plunger to expell excess air. So it doesnt affect results. Key point because we are measuring air component levels in blood.

Remove cube and needle as one.

Attach black cap to syringe.

Roll test tube between hands, to ensure blood heparinisation.

Place in iced bag. Send to lab.

Needle and cube to sharps container.

THANK YOU

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References

Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical Chemistry: Techniques, principles, Correlations. Baltimore: Wolters Kluwer Lippincott Williams & Wilkins.

Carreiro-Lewandowski, E. (2008). Blood Gas Analysis and Interpretation. Denver, Colorado: Colorado Association for Continuing Medical Laboratory Education, Inc.

Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson .

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Resources to learn more

www.acid-base.com

www.acidbasedisorders.com

Haber RJ. A practical approach to acid-base disorders. West J Med 1991; 155: 146

www.postgradmed.com/issues/2000/03_00/fall.htm

http://medicine.ucsf.edu/housestaff/handbook/HospH2002_C5.htm