Sect. 8.4 - Acid/Base Status & Disorders

kidneys

organ that plays an important role in the body's attempt to maintain a physiological pH

7.4

average pH of plasma

6.0

average pH of urine

1. Na+-H+ Exchange

2. Production of NH3 & NH4 and subsequent excretion of NH4

3. Reclamation of HCO3-

The three types of renal mechanisms that help to regulate acid-base balance

renal tubule

Where does the Na+-H+ exchange primarily occur?

Na+-H+ exchange

H+ ions are released into the tubular fluid in exchange for Na+ ions

enhanced in states of acidosis (let go of H+)

inhibited in states of alkalosis (keep H+ ions)

When is the Na+-H+ exchange enhanced and inhibited?

potassium ions compete with H+

How does potassium play a part in the Na+-H+ exchange?

more H+ ions are exchanged for Na+

If the intracellular concentration of K+ in renal tubule cells is decreased (hypokalemic states), what happens to the Na+-H+ exchange?

K+ is excreted instead of H+, which leads to a build-up of acid/H+ (acidosis)

If the intracellular concentration of K+ in renal tubule cells is increased (hyperkalemic states), what happens to the Na+-H+ exchange?

ammonia (NH3) and ammonium ion (NH4)

produced in renal tubular cells from the deamination of amino acid

pH determines which form is present

ammonia (NH3)

basic gas which readily diffuses across cell membranes

ammonium ion (NH4)

acid that cannot easily cross cell membranes and gets trapped in tubules; then gets excreted with anions in the urine

60%

NH4 (ammonium ion) production and excreted accounts for __________% of H+ asscoaited with nonvolatile acids

renal threshold is met, and the kidneys excrete bicarb into the urine

Normally, GFR filtrate has the same concentration of bicarb that plasma does. What happens when the plasma concentration is above 28 mmol/L (alkalosis)?

alkolosis

blood pH higher than 7.45

acidosis

blood pH lower than 7.35

respiratory

If the PCO2 is the parameter most out of range, it is a (respiratory / metabolic) disorder

metabolic

If the HCO3- is the parameter most out of range, it is a (respiratory / metabolic) disorder

primary

a disorder is considered _________ if the imbalance results from PCO2, HCO3-

mixed acid-base disorders

disorders that are a result of more than one pathological process occurring in an individual

compensation

body trying to return pH toward normal whenever an imbalance occurs

alters the factor not primarily affected by the pathological process

How does the body accomplish compensation?

kidneys selectively excreting or reabsorbing anions & cations (HCO3-)

If imbalance is of respiratory origin (CO2), compensation is accomplished by

lungs altering the degree of ventilation (PCO2)

If imbalance is of metabolic origin (HCO3-), compensation is accomplished by

full compensation

compensation is occurring and has successfully reached the ideal pH range of 7.35-7.45

partial compensation

compensation is occurring but has not successfully reached the ideal pH range of 7.35-7.45

respiratory compensation

this type of compensation is often immediate, but partial

metabolic compensation

this type of compensation is often slow, but complete/full

does not fix primary disease, just a temporary fix

Does compensation fix the disease?

Na+ and Cl- levels

Anion gap

HCO3-

PCO2

pH

Important indicators in the assessment of acid-base imbalance include (5):

Na+ and Cl- levels

Anion gao

HCO3-

3 indicators important early in the assessment (w/o using ABG)

10-20 mmol/L

anion gap reference range

metabolic acidosis

What does an increased anion gap indicate?

addition of acid (ketoacidosis, lactic acidosis), ingestion of toxins, and kidney failure

common causes of increased anion gaps

may also be associated with metabolic acidosis

What does a normal anion gap indicate?

loss of base (renal tubular disease, loss of bicarb from diarrhea, or the use of carbonic anhydrase inhibitors)

common causes of a normal anion gap associated with metabolic acidosis

uncommon, usually a lab error

What does a decreased anion gap indicate?

HCO3-

used to assess the metabolic component of acid-base disorders, whether the cause is primary metabolic disorder or compensation for respiratory disorder

PCO2

used to assess respiratory component of acid-base disorder

arterial blood samples

recommended sample to evaluate oxygenation

metabolic acidosis

a base (HCO3-) deficient disorder that results from either an accumulation of fixed acids or loss of extracellular buffers

causes of Metabolic Acidosis

Diabetic ketoacidosis

Uremia

Renal tubular acidosis

Lactic acidosis

GI loss of HCO3-, fluid and potassium

Exposure to toxins

pH decreased

HCO3- decreased

Lab findings in metabolic acidosis

lungs will attempt to get rid of CO2 by hyperventilation (Kussmaul breathing)

How does the body compensate for metabolic acidosis?

kidneys retain HCO3-

If kidneys are functioning, how do they help compensate for metabolic acidosis?

metabolic alkalosis

primary excess of HCO3-

can result form:

- addition of a base to the body

- decreased in amount of base leaving body

- loss of acid-rich fluids

causes of Metabolic Alkalosis

GI losses (most commonly chloride)

Renal losses

Use of diuretics (loss of H2O and all electrolytes)

Liver cirrhosis (accumulation of NH3)

Blood transfusion

pH increased

PCO2 normal

HCO3- increased

K+ & Cl- decreased

Lab findings in Metabolic Alkalosis

lungs will attempt to retain CO2 by slowing down breathing

How does the body compensate for metabolic alkalosis?

kidneys will decrease Na+-H+ exchange, formation of ammonia, and concentration of HCO3-

If kidneys are functioning, how do they help compensate for metabolic alkalosis?

respiratory acidosis

an increase in PCO2 and pH below normal

HCO3- may be normal/increased

defect in excretion of CO2, so person retains CO2

The hallmark of respiratory acidosis

causes of Respiratory Acidosis

Results from hypoventilation:

- suppression of respiratory center (meds, trauma, sleep apnea)

- weakened diaphragm

- airway problems/obstruction

- abnormal ventilation-perfusion ratio (emphysema and circulatory impairment from cardiac output).

hypoventilation

Clinically, respiratory acidosis results from

**hint: acidosis = retaining CO2

hypoxia

What is always associated with respiratory acidosis?

pH low

PCO2 increased

HCO3- normal/increased

Lab findings in Respiratory Acidosis

drowsiness, restlessness, tremors

an acute rise in PCO2 levels leads to

stupor and coma

PCO2 levels >80 mmHg often result in

brain function

modified especially when PCO2 rises acutely because the entry of CO2 in the brain is not accompanied by a concurrent rise in blood levels of HCO2

kidneys retain HCO3- and excrete H+ and Cl-

How does the body compensate for respiratory acidosis?

compensation of Respiratory Acidosis

- H+ excreted/eliminated in the form HCl and ammonium chloride (NH4Cl)

- Cl- reduced due to chloride shift

- Na+ retained by kidney to combine with elevated HCO3-

- NH4 formation increased & excreted through urine

lungs will increase breathing

If lungs are functioning, how do they help compensate for respiratory acidosis?

respiratory alkalosis

reduction in PCO2 below normal and an increase in blood pH

hyperventilation

major contributory cause of respiratory alkalosis

causes of Respiratory Alkalosis

- Conditions of Hypoxemia (pulmonary disease, congestive heart disease, severe anemia, and high-altitude exposure)

- Conditions that stimulate medullary respiratory center (hyperventilation syndrome, salicylate intoxication, pregnancy, and neurological disorders)

- Excessive mechanical ventilation

s/s of Respiratory Alkalosis

Shortness of breath

Sense of chocking

Dizziness

Nervousness

Altered level of consciousness

Eventually tetany (muscle freezing up)

pH increased

PCO2 decreased

Lab findings of Respiratory Alkalosis

Buffer system makes more H+ available to combine with HCO3 and form carbonic acid (H2CO3)

Kidneys excrete NH4 and retain Cl-

How does the body compensate for respiratory alkalosis?

Chronic Obstructive Pulmonary Disease

What does COPD stand for?

COPD

irreversible structural changes in the lungs that cause problems with ventilation and specifically an inability to exhale air rapidly

causes of COPD

long-term cigarette smoking

severe asthma

inhalation of toxic gasses

some lung autoimmune diseases

CO2 retention

COPD pts are at risk of developing _________

Alveolar ventilation is inadequate to maintain normal PCO2 levels. As compensation, kidneys retain HCO3- which causes long-term increase of CO2 and HCO3-

Emphysema and Chronic Bronchits

2 types of COPD diseases

respiratory drive

stimulated by abnormal pH and CO2 levels based on chemical receptors in CNS

increase in CO2: chemical receptors trigger an increase in respirations

What triggers respiratory drive?

hypoxic drive

receptors located within the carotid and aortic vessels

PCO2 levels fall below 55 mmHg

What triggers hypoxic drive?

10%

Hypoxic drive accounts normally for approx _______% of total drive to breath

- so weak that unconsciousness will develop before respiratory distress is noted

true

T or F:

COPD pts who have chronically compensated elevated CO2 levels are not dependent on the hypoxic drive to breathe

emphysema

structural changes in the lung causes a loss of elasticity in terminal airways and alveoli

SA of alveoli is reduced due to loss of alveolar wall integrity & air trapping

s/s of Emphysema

thin appearance

pink skin (pink puffers)

wheezing/whistling

persistent cough

chest discomfort and pain

barrel-chested later on

chronic bronchitis

chronic airway irritation with excess mucous secretion leading to infection and obstruction

NOT corrected by increasing the work in an effort to breath

pulmonary artery hypertension and eventually right heart failure

Chronic hypoxia may lead to

s/s of Chronic Bronchitis

overweight

cyanosis (blue bloaters)

persistent cough

chest discomfort and pain

produce a lot of mucus and phlegm (whitish-green)

tired

shortness of breath

Acute Respiratory Distress Syndrome

What does ARDS stand for?

ARDS

condition of atelectasis (collapsed/airless lung) due to alveolar collapse

adult ARDS

Caused by progression from inflammatory products, which produce lung surfactant activity

Cells and collagen accumulate, causing severe scarring, poor respiratory function, and hypertension

associated with: acute pulmonary injury from aspiration/infectious pneumonia, shock, burns, near-drowning

infant ARDS

premature lungs and their lack of surfactant coating the alveolar epithelium

surfactant

responsible for reducing surface tension in the alveolar wall during exhalation

alveoli collapse during exhalation

What happens if surfactant production is insufficient?

surfactant (prior to and at birth)

treatment of infant ARDS

cyanide posioning

rare, but serious condition caused by exposure to cyanide gas

burning plastic or synthetic materials in industrial setting (firefighters, farmers who burn their fields)

sources of exposure of cyanide gas

cellular hypoxia, respiratory failure, possible coma and death from heart failure

What are some effects from cyanide gas exposure?

Ferrous (Fe2+) hemoglobin

Cyanide binds to _________________ , therefore it cannot bind to oxygen.

bitter almonds

What is the characteristic odor of patients exposed to cyanide gas?

colorimetric end-point

How is cyanide most commonly measured?

pyridine-barbituric acid

What reagent is used in measurement of cyanide?

carbon monoxide (CO) posioning

odorless gas that is produced as a byproduct of the incomplete combustion of carbon

burning natural gas, gasoline, other petroleum products