Acid – Base Imbalances

Acid Base Disturbances are important because they help

-Identification of specific disturbance is important in identifying the underlying cause of the disorder

-Assists in determining treatment

Acid Base Disturbances Results provide information on the following

-Alveolar ventilation

-Oxygenation

-Acid-base balance

Decision to Obtain an ABG is made the moment

-The moment you suspect respiratory is compromised

- a patient comes in with DKA

Indications for Ordering an ABG

–when it will change your management for a particular patient

-When there are concerns about VENTILATION (are they breathing enough?)

-When there are concerns about OXYGENATION (when O2 saturation/pulse oximetry doesn’t suffice)

-When there are concerns about ACID-BASE BALANCE

do not get a ABG when

you will be doing something regardless of what the ABG shows (e.g. if the patient is not breathing and needs to be intubated, tube first, check ABG later)

what are concerns about VENTILATION

-are they breathing enough?

-Not awake enough to breathe

-Obtunded COPD patient (due to hypercarbia)

-To verify no hypercarbia in a patient with altered mental status/obtunded

-Breathing too fast/concern for poor gas exchange or muscle fatigue

-Anxious asthmatic/COPD patient breathing fast

-Septic patient breathing fast with concern for "tiring out"

You should always get ____ unless _____

-baseline

-contraindicated

restlessness/ anxiety increased means

-resp is compromised

-need ABG baseline

-not enough ventilation/oxygenation

if patient needs to be intubating what do we do first

-intubate first

-ABG after

When there are concerns about OXYGENATION (when O2 saturation/pulse oximetry doesn’t suffice)

-Concern for Carbon Monoxide Intoxication carboxyhemoglobinemia

on day of discharge what does the PO2 need to be to qualify for home oxygen

-On day of discharge to verify PO2 < 60, for the patient to qualify for home oxygen

-If there is no Arterial Line, radial arterial sticks HURT and can result

in blood vessel injury. Do it only when you need it

When there are concerns about ACID-BASE BALANCE

-Sepsis

-DKA

-Poly-drug overdose

-Increased anion gap or decreased bicarbonate on chemistries without obvious cause

-To assess "adequacy of resuscitation" in both sepsis and trauma (Lactic Acid may be substituted for ABGs)

Miscellaneous reasons to get ABG

-After intubation in all patients

-To monitor progression of disease or response to therapy in vented ICU patients or COPD patients on BiPap/after other interventions.

-During the "Apnea Test" to determine brain death

-To assess for candidacy for extubation as one of many criteria (ABG not required in every patient)

for rapid (<10 minutes)

assessment of sodium, potassium, chloride, ionized calcium ("ABG Plus")

When NOT to get an ABG

-Oxygenation alone, for the most part, can be assessed by oxygen saturation in most cases

- Keep in mind that you maintain your O2 Sat while you get

hypercarbic

-"Routine" management of vented patients in the ICU

-If you will be performing an indicated procedure regardless of the result (i.e. if the patient needs to be intubated, tube them and get an ABG afterward)

How is Acid-Base Regulated?

-Homeostatic mechanisms keep pH within normal range

-Buffer systems

-Kidneys

-Lungs

pH

-Measurement of acid or base(alkali) of a solution based on the amount of hydrogen ions available

-On a scale of 0-14

-7.0 is neutral

-< 7.0 is an acid

-> 7.0 is a base(alkali)

Blood pH is

slightly alkali with a normal range of 7.35-7.45

PH incompatible with life

pH <6.8 or >7.8

Maintain acid in body fluid

-Carbonic acid

-H₂C03

Maintain base in body fluid

-Sodium bicarbonate

-NaHc03

BUFFER SYSTEMS

-RESPIRATORY

-RENAL

Intracellular Buffers

-Exchange of hydrogen & potassium through cell membrane

-Both of these cations repel each other

-Acidemia (excess acid in blood)

-with >H+ leads to a shift of K from cells & ↑ plasma K

-Alkalemia (loss of acid or excess base in blood)

-With < H+ leads to a ↓plasma K

as nurses when we see abnormal ABG results we always must determine the

-underlying cause

which compensates faster?

respiratory compensates way faster than renal

RESPIRATORY BUFFERS

Lungs

-Removal or retention of C02

what controls respiration

medulla

RENAL BUFFERS

-Kidneys have ability to excrete or retain hydrogen ions

-Carbonic acid breaks down into hydrogen and bicarbonate in the blood

-This enters the renal tubules

-Renal compensation is relatively slow

how long do kidneys take to compensate

-hours or days

If an imbalance is caused by metabolic processes what begins to compensate

-respiratory system attempts to compensate

If an imbalance is caused by respiratory processes what begins to compensate

- metabolic (renal) system compensates

pH normal

7.35 - 7.45

PaCO2

35-45 mmHg

HCO3

22-26 mEq/L

PaO2

80-100 mmHg

SaO2

92-100%

you need the ABG

FAST

tets to check for artery patency before getting ABG

allens test

pH > 7.4

alkalosis

pH < 7.4

acidosis

respiratory acidosis Clinical manifestations

-decreased LOC

-tachycardia

-tachypnea

-hyperkalemia

-Increased BP

-Fullness in head

-Mental cloudiness

-Cerebral Vasodilation

what are the neuro affects of respiratory acidosis

-Fullness in head

-Mental cloudiness

-Cerebral Vasodilation

-decreased LOC

what are the BP affects of respiratory acidosis

-HTN

what happens to heart and respiratory rate is respiratory acidosis

-tachypnea

-tachycardia

what happens to potassium levels in respiratory acidosis

hyperkalemia

Etiology of resp acidosis

-Diseases that impair respiratory muscles

-Aspiration

-Overdose of sedatives

-Sleep apnea

-Pneumonia

-COPD

what do you give do if a patient comes in with these sx

-oxygen

-ABG test

Respiratory Acidosis

med management is directed at

-Treatment directed at improving ventilation and treating underlying cause

what are the meds you give for a respiratory acidosis pt

-Bronchodilators

-Antibiotics

-Thrombolytic

what other interventions are done for a patient with respiratory acidosis

-Adequate hydration

Supplemental oxygen (humidified)

Respiratory Alkalosis Carbonic acid deficit

-pH > 7.45

-Pac02 < 38 mm Hg

-Caused by hyperventilation

-"Blowing off C02"

-Carbonic acid deficit

Respiratory Alkalosis, CM

-Lightheadedness

-Cerebral vasoconstriction

-Inability to concentrate

-Numbness/tingling

-Tachycardia

-Arrhythmias

What are the neuro effects of respiratory alkalosis

-Lightheadedness

-Cerebral vasoconstriction

-Inability to concentrate

-Numbness/tingling

what are the CV effects of respiratory alkalosis

-Tachycardia

-Arrhythmias

ETIOLOGY OF RESPIRATORY ALKALOSIS

-Extreme anxiety

-Hypoxemia

-Cerebral tumors

-Early phase of salicylate toxicity

-Gram negative bacteremia

Respiratory Alkalosis

medical management

-Treatment depends on underlying cause

-Paper bag breathing

-Sedation

Metabolic Acidosis Base bicarbonate deficit

Definition

-pH < 7.35

-Bicarbonate level < 22 mEq/L

-Secondary to loss of bicarbonate or gain of hydrogen ion

cardinal features for metabolic acidosis

-Decrease in serum bicarbonate

-Hyperkalemia

Metabolic Acidosis CM

-Headache

-Confusion

-Drowsiness

-N/V

-Peripheral Vasodilation

-Hypotension

-Cold/clammy skin

-Arrhythmias

-Shock

-Decreased cardiac output

metabolic acidosis neuro CM

-Headache

-Confusion

-Drowsiness

metabolic acidosis GI effects

N/V

Metabolic acidosis BP effects

-Peripheral Vasodilation

-Hypotension

-Cold/clammy skin

metabolic acidosis CV effects

-Arrhythmias

-Shock

-Decreased cardiac output

metabolic acidosis etiology

-diarrhea

-diuretics

-dyalisis

-TPN

which lab do you monitor for metabolic acidosis

-electrolytes potassium

-initially hyperkalemia and then hypokalemia when you begin to correct it

metabolic acidosis Medical Management

-Correct metabolic imbalance

-Close monitoring of potassium level

–Initially hyperkalemic

–Potassium moves back into cell with correction of acidosis→causes hypokalemia

-Bicarbonate administration if necessary

Metabolic Alkalosis Base bicarbonate excess

-pH > 7.45

-Hc03 > 26 mEq/L

-Results from gain of bicarbonate or loss of hydrogen ion

-PaC02 ↑ as lungs attempt to compensate

metabolic alkalosis CM

-Tingling

-Dizziness

-Hypertonic muscles

-Symptoms of hypocalcemia

etiology of metabolic alkalosis

-Vomiting

-Excessive NGT suctioning (loss of hydrogen and chloride ions)

-Hypokalemia

-Diuretic therapy

metabolic alkalosis Medical Management

-Correct the underlying disorder

-Volume replacement with sufficient chloride

-Potassium administration