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Denver School of Nursing – ADN & BSN Programs Lecture: Fridays 3:00pm – 9:00pm No Laboratory component for this class. Pathophysiology. BIO 206 & 308 – Ch 4 – pH & Fluid Balance. CH 4. Fluid, Electro, pH Balance. Distribution of Body Fluids - PowerPoint PPT Presentation
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Denver School of Nursing ADN & BSN Programs Lecture: Fridays 3:00pm – 9:00pm No Laboratory component for this class BIO 206 & 308 Ch 4 – pH & Fluid Balance
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Page 1: Pathophysiology

Denver School of Nursing – ADN & BSN ProgramsLecture: Fridays 3:00pm – 9:00pmNo Laboratory component for this class

BIO 206 & 308 – Ch 4 – pH & Fluid Balance

Page 2: Pathophysiology

Distribution of Body FluidsTotal body water – all fluids 60% of weight

Intracellular fluid (ICF) 2/3 TBWExtracellular fluid (ECF) 1/3 TBW Interstitial fluid – between cells Intravascular fluid – blood plasma Lymph, synovial, intestinal, CSF, sweat, urine,

pleural, peritoneal, pericardial and intraocular fluid

Page 3: Pathophysiology

“Cells live in a fluid environment with electrolytes and acid base concentrations maintained within a narrow range”

changes or shifts → radically alter metabolism → life threatening

Page 4: Pathophysiology

Sodium (Na+) Primary ECF cation Regulates osmotic forces Role▪ Neuromuscular irritability, acid-base balance,

cellular reactions, and membrane transport

Chloride (Cl-) Primary ECF anion Provides electroneutrality

Page 5: Pathophysiology
Page 6: Pathophysiology

Sodium and Water BalanceBalance between Na+ and H2O - ↑ or ↓ of salt↑ or ↓ water

Tonicity – change in concentration of solutes (salt) with relation to solvent (water)

Page 7: Pathophysiology

Tonicity (280 – 294m Osm) Isotonic – 0.9% NaCl – iso osmolar

imbalance no change in cells Hypertonic – ECF > 0.9% NaCl – (↓

H2O or ↑ salt) cells shrink Hypotonic – ECF < 0.9% NaCl (↑ H2O

or ↓ salt) cells swell“Extracellular Fluid”- interstitial space

Page 8: Pathophysiology

90% ECF cations135 – 145 mEq/L

Hypernatremia - > 145 mEq/L

Hyponatremia - < 135 mEq/L

Page 9: Pathophysiology

Hypernatremia-causes• ↑ Na or ↓ H2O• IV therapy – acidosis (NaHCO3)Cushing's Syndrome - ↑ ACTH → aldosterone

fever, respiratory infection - ↓ H2Odiabetes, diarrhea - ↓ H2O ↓ H2O intake - coma

• H2O movement ICF → ECF(interstitial)• Manifestations– Intracellular dehydration: convulsions, thirst,

fever, muscle twitching, hyperreflexia

Page 10: Pathophysiology

Hyponatremia ↓ Na or ↑ H2O Vomiting, diarrhea, GI suction, burns,

diuretics, D5W replacement (isotonic sol’n)

Manifestations Lethargy, confusion, depressed reflexes,

seizures, coma, hypotension, tachycardia, ↓ urine output

Page 11: Pathophysiology

Hypochloremia

Result of hyponatremia or ↑ HCO3

Vomiting – loss HCl

Cystic fibrosis

Page 12: Pathophysiology

Potassium (resting potential) Major intracellular electrolyte 98% intracellular – Na – K – ATP Pump 3.5 – 5.0 mEq/L Transmission and conduction of nerve

impulses, normal cardiac rhythm, skeletal and smooth muscle contractions: “action potentials”

“Da BAD BOY of ELECTROLYTES”

Page 13: Pathophysiology

Potassium Levels Change in pH affects K+ balanceAcidosis causes:

↑ ICF H+ → K+ moves out to ECF maintains + ion balance

Aldosterone; insulin, epinephrine Alkolosis causes:

K+ → into cell Glucagon # entry into cell

Glucocorticoids → K+ excretion

Page 14: Pathophysiology

Hypokalemia K+ < 3.5 mEq/L ↓ intake, ↑ loss, ↑ entry into cells Manifestations: membrane

hyperpolorizations ↓ excitability – weakness, smooth muscle, atrophy, cardiac dysrhythmias (bradycardia…asystole)

Page 15: Pathophysiology

HyperkalemiaK+ > 5.0 mEq/L – rare

↑ shift from ICF (acidosis), ↓ renal excretion, insulin deficiency or cell trauma

Page 16: Pathophysiology

Hyperkalemia Mild attacks

↑ neuromuscular irritability – tingling of lips & fingers, restlessness, intestinal cramps – diarrhea

Severe attacks No repolarization → muscle weakness, ↓ tone,

flaccid paralysis Cardiac dysrhythmias “funky chicken”

Page 17: Pathophysiology

Calcium (threshold potential) 99% located in bone – hydroxyapatite Bone, teeth, blood clotting, hormone

secretion, cell receptor function Hypo - ↓ block of Na into cell ↑

neuromuscular excitability (muscle cramps) Hyper - ↑ block Na - ↓ neuromuscular

excitability (muscle weakness, cardiac arrest, kidney stones, constipation)

Page 18: Pathophysiology

Hypo - ↓ block of Na into cell

↑ neuromuscular excitability (muscle cramps)

Source: Review of Clinical Signs, Dr. Frank Urbano MD 2007.

Page 19: Pathophysiology

Low SERUM K...decreased excitability Nerves & muscles…bradycardia---asystole

High SERUM K …increased excitability Cardiac dysrhythmias

Low SERUM Ca… increased excitability “Chvostek & Trousseau’s Signs”

High SERUM Ca… decreased excitability

Page 20: Pathophysiology

pH (0 to 14) Inverse logarithm of the H+ concentration -

0.0000001 mg/L – 1x10 -7

so pH = 7 pH = power of hydrogen pH changes by one unit (7 → 6)

[H+] 10 fold Biological fluids

pH < 7.4 = acidic > 7.4 = basic

Physiologic Range of Blood pH = 7.35-7.45

Page 21: Pathophysiology

pH Acids are formed as end products of

protein, carbohydrate and fat metabolism

Narrow “life range” – 7.35 – 7.45 Bone – lung – kidneys – major regulatory organs

“Absolute Range of Life:6.8-7.8”

Page 22: Pathophysiology

pHBody acids exist in two forms

Volatile H2CO3 (maybe eliminated as CO2)

Nonvolatile – eliminated by kidneys sulfuric, phosphoric

Page 23: Pathophysiology

Image from: http://www.answers.com

Page 24: Pathophysiology

Image from: http://www3.oes.edu & http://www.fitnessspotlight.com

Page 25: Pathophysiology

Image from: http://www.getfit4kidz.com/

Page 26: Pathophysiology
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Page 28: Pathophysiology

Water Movement Between ICF and ECF“water, nutrients and waste products”

capillary interstitial space• #1 Capillary hydrostatic pressure • blood pressure “fluid out”

• #2 Capillary oncotic pressure • water attraction “fluid in”(Plasma Proteins)

• #3 Interstitial hydrostatic pressure • fluid towards capillary

• #4 Interstitial oncotic pressure • water attraction “fluid in”

Page 29: Pathophysiology

water movement

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Page 30: Pathophysiology

Edema!!

Page 31: Pathophysiology

Edema: 4 Major Causes“excessive accumulation of fluids within the

interstitial space”

1)↑ hydrostatic pressure Venous obstruction – DVT, hepatic obstruction Salt and water retention – heart, renal failure

2)↓ plasma oncotic pressure ↓ albumin – liver disease, malnutrition, kidney

disease, burns, hemorrhage

Page 32: Pathophysiology

3)↑ capillary permeability – trauma, burns, neoplastic and allergic reactions

4) Lymph obstruction – removal of nodes (surgery), inflammation or tumors

Page 33: Pathophysiology

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Page 34: Pathophysiology

From your A&P sources…

What are the two most important body systems for fluid, Electrolyte, and pH balance??

Page 35: Pathophysiology

What are the two most important regulatory systems for fluid, electrolyte and pH balance?

1) 2)

When the Blood pH is low, it is called? When the Blood pH is high, it is called?

Page 36: Pathophysiology

1) Metabolic Acidosis

2) Metabolic Alkalosis

3) Respiratory Acidosis

4) Respiratory Alkalosis

Much more detail to come latter in the lecture…

Page 37: Pathophysiology

Image from: http://academic.kellogg.edu

Page 38: Pathophysiology

Image from: http://academic.kellogg.edu

Page 39: Pathophysiology

Physiology of the Urinary System: Renal function▪ Filtration▪ Reabsorption▪ Secretion

Regulation of Urine Volume▪ Renin Angiotensin Aldosterone system

(RAAS)

Page 40: Pathophysiology

Image from: http://www.answers.com

Page 41: Pathophysiology

Sodium, Chloride & Water Balance

“kidneys and hormones” – central roleWater : ADH – hypothalamus –

posterior pituitary

Na+ and Cl- aldosterone – adrenal gland Natriuretic hormones– atrial muscle

Page 42: Pathophysiology
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Page 45: Pathophysiology

Physiological pH Control Systems- (p.1003 of our text)

Type Response Time Example“Chemical buffer systems”

Immediate 1) Bicarbonate buffer system

2) Phosphate buffer system

3) Protein buffer system

“Physiological buffer systems”

a) Minutes

a) Hours

a) Respiratory Response system

b) Renal response system

Page 46: Pathophysiology

Source: http://www.mpoullis.net

~ All body fluids, inside or outside cells have buffers which defend the body against pH changes~ The most important buffer in extracellular fluids, including blood, is a mixture of carbon dioxide (CO2) and bicarbonate anion (HCO3)~ CO2 acts as an acid (it forms carbonic acid when it dissolves in water), donating hydrogen ions when they are needed~ HCO3 is a base, soaking up hydrogen ions when there are too many of them~ The HCO3/CO2 buffer system is extremely important because it can be rapidly readjusted in alkalosis and acidosis~ There are also other buffers in blood, such as proteins and phosphate~ The ability to resist pH change is given by the buffer capacity, which is a function of the concentration and dissociation constant (pK) of the weak acid~ If there is more than one buffer in the solution, the buffer capacities are additive

The Chief Blood Buffer is a Mixture of Bicarbonate and Carbon Dioxide

Page 47: Pathophysiology

Source Mayo Clinic: http://discoverysedge.mayo.edu

Page 48: Pathophysiology

Source: http://www.mpoullis.net

The Chief Blood Buffer is a Mixture of Bicarbonate and Carbon Dioxide

Page 49: Pathophysiology

Source: http://www.mpoullis.net

~ The balance will swing toward a low pH, producing acidosis~ Pathology leading to this Acidosis can be:

1) CO2 increase via hypoventilation (pneumonia, emphysema)

2) Metabolic conditions (ketoacidosis due to excess fat metabolism

(diabetes mellitus) which will lower bicarbonate.

Too Much CO2 or Too Little HCO3 Will Cause Acidosis

Page 50: Pathophysiology

Source: http://www.mpoullis.net

~ The balance will swing toward a high pH, producing alkalosis~ Pathology leading to this Alkalosis can be:

1) CO2 decrease via hyperventilation (Remember Respiration “Blows off CO2”)

2) Emesis removed stomach acid and raises bicarbonate (Alkalosis is clinically less common than acidosis)

Too Much HCO3or Too Little CO2 Will Cause Alkalosis

Page 51: Pathophysiology

Buffer is a chemical that binds XS H+ or OH- without a significant change in pH

Consists of a PAIR of a weak acid and its conjugate base

Most important plasma buffering system 1. Carbonic acid – bicarbonate system2. Hemoglobin (intracellular)

Page 52: Pathophysiology

H2O + CO2 H2CO3 H+ + HCO3-

1 20 Lung Kidney Phosphate- HPO4Ammonia – NH3 Compensation Respiratory - ↑ or ↓ CO2 Renal - ↑ or ↓ acidity / alkalinity of urine

Correction – buffer pairs →

Page 53: Pathophysiology

Other Systems not previously discussed Proteins: - charge, mostly intracellular

Hemoglobin –H + Hb → HHb + CO2 → HHbCO2 (weak acid)

.

Page 54: Pathophysiology
Page 55: Pathophysiology

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Figure 4-10 (p. 116)

Page 56: Pathophysiology
Page 57: Pathophysiology

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Figure 4-11 (p. 117)

Page 58: Pathophysiology
Page 59: Pathophysiology

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Figure 4-12 (p. 117)

Page 60: Pathophysiology
Page 61: Pathophysiology

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Figure 4-13 (p. 118)

Page 62: Pathophysiology
Page 63: Pathophysiology

1) Metabolic Acidosis – Different diseases such as untreated diabetes mellitus or during starvation, the blood pH becomes acidic because there is higher carbonic acid to bicarbonate ratio. This stimulated the respiratory centers to increase respiratory rate and thus “blow off” carbon dioxide. The kidneys will also excrete increased levels of H ions and NH3. If these mechanisms can not compensate then the pathologic condition of uncompensated metabolic acidosis develops

2) Metabolic Alkalosis – Excesive use of antacids or excessive emesis can produce metabolic alkalosis. Initially the condition can result to bicarb levels up to 40 x greater than carbonic acid. Compensatory mechanisms function to increase the carbonic acid and decrease the bicarb. This is done via hypoventilation and increased renal excretion of bicarb. Once again if compensation is not adequate uncompensated metabolic alkalosis develops.

Page 64: Pathophysiology

Source: http://www.mpoullis.net

3) Respiratory Acidosis – Pneumonia, emphysema and barbiturate OD are leading causes of retention of carbon dioxide in the blood. In these conditions the carbonic acid is greater than bicarbonate buffer. The compensatory reaction is for the kidneys to excrete H ions and retain more bicarbonate.

4) Respiratory Alkalosis – Hyperventilation due to a multitude of reasons (fever or hysteria) can result in excessive loss of carbonic acid and lead to respiratory alkalosis. Once again the kidneys will attempt to compensate via increased H ion reabsorption and increased bicarbonate excretion.

Page 65: Pathophysiology

1) Metabolic Acidosis

2) Metabolic Alkalosis

3) Respiratory Acidosis

4) Respiratory Alkalosis

Page 66: Pathophysiology

pH = 7.35 – 7.45pO2 = 80 to 100 mmHgpCO2 = 35 – 45 mmHgHCO3 = 22-26 mEq/LSaO2 = > 90%

Page 67: Pathophysiology

PatientABG: pH = 7.3pCO2 = 40 mmHg pO2 = 70 mmHgHCO3 = 20 mEq/L

1. pH = ? → acidosis 2. pCO2 = ? → normal3. HCO3 = ? → low 4. pO2 = ? → low

Page 68: Pathophysiology

Patient pH = 7.30 1. pH = acidotic Pco2 = 30mm Hg 2. Pco2 = alkalotic Po2 = 68mm Hg 3. Po2 = hypoxic HCO3 = 14mEq/L 4. HCO3 = acidotic O2 sat. = 92% 5. O2 sat = low “same directions = compensation”

Metabolic acidosis with partial respiratory compensation

Page 69: Pathophysiology
Page 70: Pathophysiology

ACIDOSIS: CNS depression Stupor to confusion to coma

ALKYLOSIS: CNS irritability Restlessness to seizures

Page 71: Pathophysiology

Image Source: http://www.gilmerfreepress.net


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