ACID-BASE DISTURBANCES Acid-Base Disturbances Plasma pH indicator of hydrogen ion (H+) concentration Normal pH: 7.35-7.

-7.45 Consists of buffer systems, kidneys and lungs pH range compatible with life: 6.8-7.8 BUFFER SYSTEMS Prevent major changes in the pH of body fluids by removing or releasing H+ The bodys major EC buffer system: Bicarbonate-carbonic acid buffer Assessed in ABG CO2 is potential acid when dissolved in water Carbonic acid (CO2+H2O =H2CO3) Less important buffer systems in the ECF: Inorganic phosphates and plasma proteins IC buffers: Proteins, organic and inorganic phosphates, RBC and hgb Kidneys Regulates the bicarbonate level in the ECF Regenerate and reabsorb them from the renal tubular cells (+) respiratory and metabolic acidosis Kidneys excrete H+ and conserve HCO3 (+) respiratory and metabolic alkalosis Kidneys retain H+ and excrete HCO3 Kidneys cannot compensate for metabolic acidosis rated by renal failure Renal compensation for imbalances is relatively slow (hours or days) Lungs Under the control of medulla Control the CO2 and thus, the carbonic acid of ECF A rise in pCO2 in arterial blood is a powerful stimulant to respiration pO2 also influences respiration, but not as marked as CO2 (+) Metabolic acidosis Inc RR elimination of CO2

(+) Metabolic alkalosis dec RR CO2 retained

ACUTE AND CHRONIC METABOLIC ACIDOSIS (BASE BICARBONATE DEFICIT METABOLIC ACIDOSIS Low pH, low HCO3, Gain of H+ or loss of HCO3 2 Forms: According to the values of serum anion gap High anion gap acidosis Normal anion gap acidosis Anion Gap: reflects normally unmeasured anions; not all electrolytes are measured Anion gap=Na+ + K+ - (Cl+ HCO3) Normal: 12-16 mEq/L (12-16 mmol/L) Anion gap=Na+ - (Cl- + HCO3-) *** Normal: 8-12 mEq/L (812 mmol/L) >16mEq/L (16mmol/L) excessive accumulation of unmeasured anions Anion Gap: 2 Forms High Anion Gap Acidosis Excessive accumulation of fixed acid Ketoacidosis, lactic acidosis, late phase of salicylate poisoning, uremia, ketoacidosis with starvation Normal Anion Gap Acidosis Results from direct loss of HCO3 Diarrhea, lower GI fistula, use of diuretics, renal insufficiency, excessive Cl, administration of parenteral nutrition without HCO3 Also referred to as hyperchloremic acidosis Reduced or Negative anion gap caused by hypoproteinemia CLINICAL MANIFESTATIONS pH <7 Headache, confusion, drowsiness, inc RR and depth, n/v, peripheral vasodilation and dec CO Dec BP, cold, clammy skin, dysrhythmias and shock

ASSESSMENT AND DIAGNOSTIC FINDINGS HCO3- <22mEq/L Low pH <7.35 (+) Hyperkalemia (+) Hyperventilation Calculation of anion gap to determine the cause ECG (+) dysrhythmia caused by hyperK+ MEDICAL MANAGEMENT Eliminate the source of chloride Administer HCO3 Serum K+ level is monitored closely Chronic metabolic acidosis: low serum Ca+are treated first to avoid tetany Alkalyzing agents Hemodialysis or peritoneal dialysis ACUTE AND CHRONIC METABOLIC ALKALOSIS (BASE BICARBONATE EXCESS) High pH and high plasma HCO3 Gain of bicarbonate or loss of H+ Most common cause: Vomiting or gastric suction Also occurs in pyloric stenosis Associated with loss of K+ (diuretics and excessive adrenocorticoid hormones such as hyperaldosteronism and Cushings syndrome) Excessive alkali ingestion from antacids containing bicarbonate during CPR Chronic metabolic alkalosis occurs with long term diuretic therapy Clinical Manifestations Dec Ca+ (more Ca+ combines with proteins) tingling of the fingers and toes, dizziness and hypertonic muscles RR is depressed (compensatory) (+) HypoK+ Atrial tachycardia, ventricular disturbances Dec motility and paralytic ileus Assessment and Diagnostic Findings

ABG: pH >7.45, HCO3 >26mEq/L pCO2 inc compensate Hyopoventilation semiconscious, unconscious or debilitated pxs (+) hypokalemia Medical Management Sufficient chloride must be supplied for the kidney to absorb Na+ with Cl- allows excretion of HCO3 NaCl fluids KCl H2receptor antagonist reduce production of HCl Carbonic anhydrase inhibitor for pxs who cannot tolerate rapid volume expansion Monitor I/O

ACUTE AND CHRONIC RESPIRATORY ACIDOSIS (CARBONIC ACID EXCESS) pH <7.35 and pCO2 >45 Causes: Inadequate excretion of CO2 Inc carbonic acid dec pO2 Emergency situations: Pulmonary edema, aspiration of foreign object, atelectasis, pneumothorax, overdose of sedatives, administration of O2 in pxs with hypercapnia, severe pneumonia and ARDS Disease that impairs respiratory muscles (muscular dystrophy, MG and GBS)

Clinical Manifestations VF 1st sign Inc PR, RR, BP Mental cloudiness, feeling of fullness in the head Inc pCO2 cerebral vasodilation inc cerebral bld flow inc ICP papilledema Chronic resp acidosis Emphysema and bronchitis, Obstructive sleep apnea, obesity

Assessment and Diagnostic Findings pH <7.35, pCO2 >45 Monitor serum electrolytes CXR Drug screen overdosage ECG Medical Management Improve ventilation Bronchodilators Antibiotics Thrombolytics or anticoagulants for pulmonary emboli Pulmonary hygiene measures Adequate hydration (23L/day) Supplemental O2 Mechanical ventilation Semi-fowlers position pCO2 above 50mmHg Hypoxemia becomes the major drive for respiration Medulla become insensitive to CO2 O2 O2 should be administered with caution Px develops CO2 narcosis Removes the stimulus of hyoxemia

Lightheadedness d/t vasoconstriction and dec cerebral bld flow Inability to concentrate, tinnitus loss of consciousness Numbness and tingling dec Ca+ Tachycardia and atrial dysrhythmias Assessment and Diagnostic Findings ABG Evaluate serum electrolytes Dec K+ Dec Ca+ Dec PO Toxicology screen r/o salicylate toxicity Medical Management (+) Anxiety Breathe slowly or breathe to a close system (paper bag) Sedative

MIXED ACID-BASE DISORDERS Patient can simultaneously experience 2 or more independent acid-base disorders A normal pH + change in pCO2 and HCO3 = Mixed disorder The only mixed disorder that cannot occur mixed respiratory acidosis and alkalosis Example: Simultaneous metabolic acidosis and respiratory acidosis (cardiac arrest) COMPENSATION Pulmonary and renal systems compensate for each other Lungs compensate for metabolic disturbances by changing CO2 excretion Kidneys compensate for respi distrubances by altering HCO3 retention and H+ secretion

ACUTE AND CHRONIC RESPIRATORY ALKALOSIS (CARBONIC ACID DEFICIT) pH >7.45, pCO2 <35 Always due to hyperventilation Causes: Extreme anxiety, hypoxemia, early phase of salicylate toxicity, gram negative bacteremia and inappropriate ventilator settings Chronic: Chronic hypocapnia, dec HCO3 Chronic hepatic insufficiency and cerebral tumors Clinical Manifestations

Acid-Base Disturbances and Compensation

Steps in Assessing ABG First, note the pH pH >7.5 alkalosis pH <7.5 acidosis pH 7.5 Normal Next step, determine the primary cause of disturbance by evaluating the CO2 and HCO3- in relation to the pH

DISORDER Respiratory acidosis

INITIAL EVENT Inc CO2, inc or normal HCO3-, dec pH Dec CO2, dec or normal HCO3-, inc pH Dec or normal CO2, dec HCO3-, dec pH Inc or normal CO2, inc HCO3-, inc pH

COMPENSAT ION Kidneys eliminate H+ and retain HCO3Kidneys conserve H+ and excrete HCO3-

Respiratory alkalosis

Metabolic acidosis

Lungs eliminate CO2, conserve HCO3Lungs dec ventilation to inc CO2, kidneys conserve H+ to excrete HCO3-

Metabolic alkalosis