acid, base, electrolyte,ph_ balance

8/13/2019 Acid, Base, Electrolyte,pH_ Balance

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Acid, Base, Electrolytes

Balance and Alterations


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Fluid Compartments


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Fluid Compartments:

20

40

60 Rule


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Fluid Movement


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Water and Electrolyte Balance

Input = output

Hormones Na+ / K+

Renin

Aldosterone ANP Reproductive Hormones GCC

Ca++ / Mg++ Calcitonin

PTH

H2O ADH

Anions follows passively

Cl- HCO3- PO4=


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Water

Intake

Loss

Normal Abnormal

Osmosis

Hormonal control

Capillary Dynamics

CHP COP

IHP IOP


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Osmosis


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Capillary Dynamics


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Capillary Pressures


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Fluid Shift to third space

Edema

Effusion

Transudate

Low cell

Low protein

Exudate

Types: Nonseptic, Septic

Contents High cell

High protein


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Edema

Causes Obstruction Overload Inflammation hypoalbuminemia

Vessels Angioedema Lymphedema

Types Localized

Pitting Weeping

Dependent Generalized


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Pulmonary Edema


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Pleural Effusion


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Terminology

Isotonic

Hypovolemia

Hypervolemia Hypertonic

Hyperosmolar

Hypotonic

Hypo-osmolar


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Functions of electrolytes


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Electrolyte Fluid Composition


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Hormones that regulate

Electrolytes

Aldosterone

ANP

PTH

Cacitriol

Calcitonin


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Cations

+ charge

Location

Function Hormonal Controls

Alterations

Hypo-

Hyper-


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Hyponatremia

< 135 mEq/L

Etiology Decreased Na+ (diet)

Increased H20 Diuretics Hiridosis Addisons Disease

DM Diarrhea CRF

Clinical Signs H20 shift to ICF Cells swell

CNS sensitive V/D Lethargy Confusion Seizures

Muscle weakness


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Hyponatremia


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Hypernatremia

> 147 mEq/l

Etiology

Excessive intake

Hyperaldosteronism Drowning (salt water)

H20 loss DI

Renal

Fever / Sweat

Burns

Diarrhea

Clinical Signs

Osmotic shrinkage

CNS sensitive

Lethargy Irritability

Hemorrhage

Seizures

Coma

Muscle weakness


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Hypokalemia

< 3.5 mEq/l

Etiology Decreased intake

ANS V/D Diuretic Sweating

Digitalis Insulin excess

Clinical Signs Decreased RMP

Heart dysrhythmia

Bradycardia AV blocks PVCs

Sphincter weakness

Delayed cardiac

repolarization ST segment depression T decreased/inverted


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Hyperkalemia

> 5.5 mEq/l

Etiology Increased intake

Insulin deficiency Hemolysis Hypoxia CRF

Diuretics Burns Extensive surgeries

Clinical Signs Inactivate Na+

channels

Muscle weakness Muscle paralysis paralysis

Cardiac dysrhythmia Peaked T wave

Widened QRS


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Hypocalcemia

< 8.5 mg/dL

Etiology Nutritional deficiency

Osteoblasticmetastasis

PTH deficiency Hyperphosphatemia

Increased proteinbinding

Chelation therapy

Clinical Signs NMJ irritability

Muscle Spasm

Dyspnea Seizures Colic Tetany

Cardiac Dysrhythmia


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Hypercalcemia

> 10.5 mg/dL

Etiology

Cancer

Hyperparathyroidism

Bone remodeling

Increased reanalfiltering

Clinical Signs

NMJ decreased Fatigue

Lethargy

Weakness

Cardiac dysrhythmia

Bone loss

Urolithiasis


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Hypomagnesemia

< 1.5 mEq/l

Seen with hypokalemia

and hypocalcemia

Etiology Decreased dietary intake

GI loss Malabsorption

Maldigestion

Diarrhea

CRF

Clinical Signs

Decreased threshold Tetany

Vertigo Nystagmus

Muscle spasms hyperreflexia

Seizures

Cardiac Dysrhythmia


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Hypermagnesemia

> 2.5 mEq/l

Etiology

Excess intake(antacids)

Decreased renalexcretion

CRF

Adrenal insufficiency

Clinical Signs

Increased thresholdfor depolarization

Muscle weakness Decreased reflexes

Hypotension

Decrease Na+ current

Cardiac dysrhythmia Bradycardia


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Anions

Chloride

ECF

Alterations

Hypochloremia

< 95 mEq/L Accompanies

hyponatremia

Severe vomiting Diuretics

Hyperchloremia

> 103 mEq/L Accompanies

hypernatremia

Phosphate

ICF, stored in bones

Alterations

Hypophosphatemia

< 2.7 mg/dL Antacid use Prolonged decrease cam

causeRickets/Osteomalacia

Hyperphosphatemia

> 4.5 mg/dL Renal failure Overuse of laxatives Hypoxia


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Acid Base Terms

Define pH Acid

Strong Weak Volatile : CO2 from CH20 and Fat Metabolism Nonvolatile: H2SO4, H2PO4 from protein metabolism

Base Strong

Weak Salt Buffer


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Acid Sources


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pH

Define pH = log (1/[H+]) pH = -log [H3O+]

Water Dissociation

H2O + H2O

H3O+ + OH-

Scale

Blood values Venous Arterial

Abnormal Values Acidemia Alkalemia


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pH formula and scale


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Acid Base Chart


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pH of Solutions


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Acid Base Regulation

for Balance

Systems Chemical Buffer Systems Respiratory System Renal

Time

Seconds to Minutes Minutes to Hours Hours to Days / Weeks

Strength

Problems (reference 7.4 as normal average):

+ / - 0.1 changes result in respiratory rate changes + / - 0.2 to 0.3 changes result in CV and Nervous changes + / - 0.4 to 0.5 changes result in death


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Chemical Buffer Systems

Define

3 types

Name of System Buffer formula or name of chemical

Location

Effectiveness [pKa buffer = pH location]

Why important


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pH changes with/without buffers


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Bicarbonate Chemical Buffer

H2CO3, HCO3-

Plasma buffer

pK = 6.1

Important:

Can measure components pCO2 = 40 mmHg HCO3- = 24 mM

Can adjust concentration / ratio of components HCO3- @ kidneys CO2 @ lungs

Recalculate pH of buffer system in ECF using Henderson-Hasselbach

pH = 6.1 + log(24 / 0.03x40) pH = 6.1 + log (20/1)

pH = 7.4


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Bicarbonate Buffer System


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Phosphate Chemical Buffer

H2PO4-, HPO4=

ICF, Urine

pK = 6.8 Important

Intracellular buffer

ICF pH = ~ 6.56.8 Renal Tubular Fluids

Urine pH ranges 6.07.0


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Proteins in acid base


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Hemoglobin


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CO2 transport and RBC buffer


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Respiratory for A/B Balance

Occurs in minutes

CO2 only Rate changes


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Respiratory Controls for

Acid /Base balance

Volatile Acid: CO2

pH changes in CSF

Respiratory Rate Pons Medulla Oblongata

Chemoreceptors

pCO2 pO2


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CO2 and pH

Increase CO2

Increase H+

Decrease pH

Decrease CO2

Decrease H+ Increase pH


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Renal Control for Long Term

Acid / Base Balance


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Renal processes in A/B balance


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Renal Physiology

Filtration Remove metabolic acids:

Ketones, Uric acid

Filter Base [HCO3-] @Renal Filtration Membrane

Reabsorption Base @ PCT Reverse CO2 equation to

create HCO3-

Secretion H+ @ PCT, late DCT and

Cortical CD CO2 equation to create H+

for secretion


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Renal Mechanisms for A/B


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Renal Buffer Mechanisms


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Normal Acid Base Values


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Respiratory and Renal Balance


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Classifying Metabolic Acid Base

Balance Problems (H+/ HCO3-)

Systems Renal Endocrine GI

Cardiovascular / Fluid administration

Metabolic Acidosis Retain Acid Lose Base

Metabolic Alkalosis Retain Base Lose Acid


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Compensation


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Adjustments for Acid/Base Balance

Imbalance

Respiratory Acidosis Incr pCO2

Respiratory Alkalosis

Decr pCO2 Metabolic Acidosis

Decr HCO3- Incr H+

Metabolic Alkalosis

Incr HCO3- Decr H+

Compensation

Increase renal acidexcretion, Incr HCO3-

Decrease renal acidexcretion, decr HCO3-

Hyperventilate to lowerpCO2

Hypoventilate toincrease pCO2


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Summary for A/B Balance


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Questions?

Water and electrolytes

acid, base, electrolyte,ph_ balance

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