1st line of defense

acts as sponges to soak up or release  h+

major buffer system is the base bicrbonate (HCO3) & carbonic acid (H2CO3).

q20x HCO3 : q1x H2CO3

this process can not maintain sustain prolonged regulation.

- the 2nd line of defense against acid-base imbalances

- the lungs role in acid-base balance involves the regulation of

CO₂

- assists when there is a fluctuation acute H+ ions concentrations

- can regulate CO2 by altering the rate & epth of RR

-  

arterial 35-45mm Hg

3rd line of defense

capable of admitting or releasing excess H+ ions

4th line of defense against acd base imbalance

- to help compensate the kidneys alter the rate of excretion of H+ & bicarbonate ions in the urine.

- responds to large or chronic fluctuations in H+ productions or elimination. 

- the most powerful regulator.

excess serum CO2 levels r/t RETENTION of CO2

e.g. Pneumonia, resp. failure, Rx OD, airway obstruction.

inc. PaCO2

inc. H2CO3

dec. in pH

resp. acidosis: Etiology

r/t mechanical or structural dec. in pulmonary ventilation

- can be classified as acute or chronic

Acute Respiratory Acidosis

-  Reduced alveolar

- Airway obstruction

- Respiratory depression

- Inadequate chest expansion

Chronic Respiratory Acidosis

- Impaired gas exchange related to trapping of C0₂ 2^° pulmonary tissue destruction (COPD)

- Chronic respiratory conditions asthma, bronchitis, emphysema, bronchiectasis

-  Dec. in pH & O2 level

- initially inc HR & CO,as it worsens HR dec. , peripheral pulses difficult to find, hypotension

- lethargy to confusion, as it worsens leads to unresponsiveness

- dec. muscle tone & deep tendon reflexes, as it worsens leads to flaccid paralysis.

- RR shallow & rapid due to reduced breathing efforts

- skin & mucous membranes are pale & cyanotic

- kidneys will eventually compensate for the imbalance.

- Drug Therapy: promotes openly airways & thins secretions-bronchodilators

- Oxygen Therapy: give O₂ at 2 liters, promotes gas exchange

-  Pulmonary Hygiene: postural drainage, deep breathing & cough, mid-high Fowler’s, inc. fluids to thing secretions

NI for Respiratory Acidosis

-  Assess LOC, vital signs, lungs sounds, mucous membranes & skin.

- mid-high Fowler’s

- ***Use pillows to support upper body in an upright position pillow in lumbar region can aid diaphragmatic excursion by exaggerating normal curvature of the spine.

- Teach Pt.to deep breath & cough

- access ABG

excessive loss of  CO2

dec. CO2

inc. pH

dec. PaCO2

etiology: Resp. alkalosis

- excessive blow off of CO2

- e.g hyperventalation, r/t stress, anxiety.

- over stim. of resp. center

- OD of ASA

- IC surgery, head injuries

- hyperventalation

- tinnitus

- dizzubess

- inability to concentrate, confusion

- hypocalcemia

- tingling sensation toes, fingers, lips, dizziness

- hyper-reflexia, muscular twitch, convulsions

lab values:

pH inc

PaCO2 dec

HCO3 normal

pH inc.

PaCO2 low

HCO3 normal

begins immediatly but not evident for 6-8hrs

Ph: normal, PaCO2 normal, HCO3 dec. 

Acid Base Mnemonic

ROME

R                                                    Resp.

O                                              Opposite 

pH inc, PCO2 dec. (ALKALOSIS)

pH dec, PCO2 inc. (ACIDOSIS)

M                                              Metabolic

E                                                   Equal

pH inc, HCO3 inc. (ALKALOSIS)

pH dec., HCO3 dec. (ACIDOSIS)

-deal c the etiology

- correct electrolyte imbalances

- assess breathing pattern

- provide emotional support, stay c Pt.

- implement re-breathin measures (paper bag over Pt. mouth)

- assess temp. HR and rhythm

-IV fluids

non-resp. acidosis

- r/t dec. in serum bicarbonate level

pH inc.

HCO3 dec.

PaCO3...

Etiology: Metabolic Acidosis

- excessive oxidation of fatty acids: DKA & Starvation.

Hypermetabolism

- excessive ingestion of acids, ETOH, methanol & salicylate.

- under elimination of H+ ions: kidney failure.

- over elimination of Bicarb: D.

- depression, HA, drowsiness, lethargy

- bradycardia, heart block, hypotension, thready peripheral pulse.

- kussmal resp.

- hyporeflexia, skeltal muscle weakness, flaccid

- vasodilation of the skin & mucous membranes

Treatment of Metabolic Acidosis

- Tx the etiology

- Correct & maintain F&E balance

- Neutralize the acid

NI: Metabolic Acidosis

-

-Assess LOC

-Assess v/s

*RR - Kussmaul breathing - deep and rapid –

-* HR & rhythm 

- *Inc. K levels - bradycardia

-safety risk

*Muscle weakness or malaise r/t changes in K

-Assess lab values

*K levels inc. as the body shifts K out of the cell trying to maintain electrical neutrality = hyperkalemia

*ABG's

-Assess I&O

*Weigh the client

*Diarrhea

- admin insulin, to restore norml. metabolism

- high intake of CHO

Metabolic Alkalosis

pH inc.

HCO3 inc

- condition of dec. H+ ions & high plasma bicarb

- acid to base is altered c an inc. in bicarb.

- Abnormal gain of bicarb or Increase in Base

- Abnormal loss of hydrogen ions or decrease in acid

- Gastrointestinal (loss of H⁺ and CL ions)      

*Vomiting

*Suctioning

Renal H⁺ loss

Diuretics

Predisposing to Metabolic Alkalosis

-Hypokalemia

- R/T Diuretic Therapy, Excessive Adrenalcorticoid Hormones,

H+ ions shift into the cells.   

S/s of Metabolic Alkalosis

- involvement develops as the pH rises

- *Irritability, dizziness, agitation, confusion

- Hypocalcemia: positive Chvostek’s & Trousseay’s signs

- Tetany, convulsions, weak hand grips, difficulty standing

- HR inc. pulse thready, pt’s on digoxin are at high risk for toxicity

- Causes CO₂ to be retained

-  dec.in K will inc. severity of metabolic alkalosis

- inc. in bicarb causes dec. in CL

Tx of Metabolic Alkalosis

-Treat the etiology

-Correct F&E imbalance

NI for Metabolic Alkalosis

Assess LOC

*Irritability, lethargy, disorientation

-VS

*Pulse - K changes affect cardiac activity

*RR - decreased rate, apnea r/t compensatory responses of lungs as pt improves assess deeper & inc. rate ventilation

-Assess BS

*May be paralytic ileus secondary to hypokalemia

-Assess I&O

*Wt changes fluid balance

*Gastric suction

**Replacement of losses

-Assess lab data

-Educate Pt. about

*Diuretics K⁺ replacement

*Taking excessive antacids