PATHO: Electrolyte Balance & Exemplars

Fluid & Electrolyte Balance definition

The various body fluids and electrolytes (intracellular, extracellular, intravascular, and transcellular) that when in balance promote homeostasis.

electrolyte imbalances

abnormal plasma concentrations of electrolytes

• deficit and excess

chloride is

main extracellular anion

chloride concentration is

proportional to sodium

• typically follows sodium

where is chloride found

in stomach

chloride is a component of

hydrochloric acid

hypochloremia causes

• Vomiting, diarrhea (lost from stomach)

• NG suctioning

• Alkalosis (acid being left)

hypochloremia signs and symptoms

• Weakness

• Headache, nausea

• Hyponatremia

• Fluid excess – cerebral edema, seizures

Hyperchloremia causes

• Dehydration

• Acidosis

Hyperchloremia signs and symptoms

• Decreased urine output

• Thirst d/t dehydration

• Hypernatremia

• Tachy

• may be asymptomatic

potassium is a

Predominant ICF electrolyte

potassium maintains

resting membrane potential

potassium abnormalites can

quickly lead to lethal complications, particularly cardiac issues

potassium and cell

potassium should be inside the cell not outside

Hypokalemia causes

• Decreased intake, GI loss thru suctioning, loop diuretics

• Fluid overload

• Alkalosis

• prolonged anorexia

Hypokalemia signs and symptoms

• Flat T waves, ST depression, v-fib

• Decreased DTRs

• Respiratory arrest

• Confusion

Hyperkalemia causes

• Renal failure

• Tissue trauma, burns

• Hypoxia

• Acidosis

• Insulin deficiency

• Results in K+ movement from ICF to ECF

Hyperkalemia signs and symptoms

• Peaked T waves, wide QRS, bradycardia, heart blocks, dysrhythmias (decreased contractility)

• Numbness, tingling

• N/V/D

where is majority of calcium found

in bone

• small amount of ionized (free) calcium bound to proteins in serum

what is calcium essential for

coagulation, muscle contraction,

what does calcium act as

messenger in some hormonal pathways

Hypocalcemia causes

• Renal failure

• Decreased PTH secretion

• Vitamin D or calcium deficiency in diet

Hypocalcemia signs and symptoms

• Tetany

• Numbness, tingling

• Hyperactive reflexes

• Positive Chvostek & Trousseau signs

• Bone pain, fractures

• Prolonged QT intervals, cardiac arrest

Hypercalcemia causes

• Malignancy

• Hyperparathyroidism, hyperthyroidism

• Immobilization

• Excessive consumption of Ca+ or Vit D (dairy, green leafy vegetables, salmon)

Hypercalcemia signs and symptoms

• Anorexia, N/V

• Muscle weakness d/t blockage of Na+ channels

• AV block

• Lethargy, coma (everything is slowed down)

PTH/ hormonal regulation and fluid electrolyte balance

hypocalcemia→ pth→ blood calcium levels rise

phosphorus role

Bone formation,

what does phosphorus act as

biffer in acid-base balance

what is phosphorus involoved in

blood cell and platelet function

phosphorus relationship

Has inverse relationship with calcium – if one is elevated, other is decreased and vice versa

Hypophosphatemia causes

• Malnutrition, alcohol abuse

• Heat stroke, burns

• Hyperparathyroidism

• Hypercalcemia

Hypophosphatemia signs and symptoms

• Joint stiffness, bone pain

• Bleeding disorders

• Seizures

Hyperphosphatemia causes

• Chronic renal failure

• Acidosis

• Hypocalcemia

• Chemotherapy

Hyperphosphatemia signs and symptoms

• Tetany (decrease in calcium= excitability)

• Decreased BP

• Cardiac dysrhythmias

magnesium is a

intracellular cation

what is magnesium regulated by

PTH

what does magnesium have a role in

ATP generation, smooth muscle relaxant

Hypomagnesemia causes

• Alcohol abuse

• Hypocalcemia

• Decreased protein

• DKA

Hypomagnesemia signs and symptoms

• Hypertension, tachycardia

• Tetany

• Cardiac dysrhythmias (PVCs, v-tach)

• Seizures

Hypermagnesemia causes

• Renal failure

• Laxative abuse

• Burns

Hypermagnesemia signs and symptoms

• Hypotension

• Lethargy

• Cardiac dysrhythmias (tall T waves, wide QRS, prolonged QT)

• Decreased DTRs

• flushing→ respiratory failure

when do burns occur

when soft tissue exposed to high-energy heat producing elements

what happens to skin functions after a burn

All functions of skin become impaired – risk for infection, sensation impairment

after a burn cells are unable to

regulate water absorption

• sodium pump fails, water and electrolytes leak out into interstitial spaces

after a burn there is loss of

circulatory volume (from loss of regulation of water absorption)

• hemoconcentration and increased blood viscosity occur

after burn what response happens

Systemic inflammatory response – cellular mediators disrupt every system

superficial burn

epidermis, sunburn

• first degree burn

superfical partial thickness

epidermis and papillary dermis involved; blistering, full pain sensation

• 2nd degree

Deep partial thickness

epidermis, papillary dermis, and reticular layer of dermis; blistering, does not blanch, no pain sensation

• 2nd degree

full thickness

all epidermal, dermal layers, and subcutaneous tissues affected; skin charred, pale, painless, need surgery

• 3rd degree

Full Thickness and Deeper Tissue

destruction of epidermis, dermis, and underlying subcutaneous tissue, tendons, muscle, and bone

• 3rd degree

• amputation probably

Zone of coagulation

area that has been completely burned

zone of stasis

fibrin deposits, vasoconstriction, may be viable

Zone of hyperemia

typically will recover, vasodilation d/t inflammation

thermal burns

scalding, radiation; occurs from a heat source

chemical burns

Direct contact, inhalation and ingestion with corrosive and caustic substances

electrical burns

passage of electrical current through the body to the ground or electrical flames or radiation; leads to internal damage along pathway of electrical charge

how to determine percent of body affected

rules of nines

burn complications

Scarring

Contractures

Hypovolemia

Infection

Inhalation Injuries – ARDS – increased mortality

Skin Graft (Donor Site)

Hypermetabolism – need proper nutrition to heal

Pain management

kidney functions

• Regulate body fluids and electrolytes

• Excrete waste products

acute kidney injury

abrupt reduction in kidney function; accumulation of nitrogenous wastes (azotemia)

acute kidney injury levels

BUN- inceased

creatinine- increased

GFR- decreased

AKI is often

reversible

prerenal AKI

reduced blood flow to the kidney

reducked arterial blood volume

intrinsic AKI

direct damage to the kidneys

postrenal AKI

obstruction of the urinary collecting system

• kidney stones, bladder tumor, prostate

AKI – Pre-renal

Decreased blood flow to kidney d/t decreased volume from hypovolemia, heart failure, or vasodilation (sepsis)

when is RAAS initiated

AKI- pre renal

what does RAAS do

increase resorption of H2O and Na+

AKI – Intrarenal/Intrinsic

Direct damage to kidneys

• Glomerulonephritis

• Nephrotoxins

• Rhabdomyolosis

when do you have greatest risk for CKD

AKI- intrinsic

AKI – Postrenal

Obstruction of urinary collecting system; cessation of urine flow

AKI – Postrenal obstructions

Tumors, kidney stones, ureteral strictures

AKI – Postrenal obstructions leads to

hydronephrosis (water/fluid in kidneys)

AKI Signs and Symptoms

• Rise in BUN, urea, & creatinine

• Decreased GFR and urine output

• Edema

• Electrolytes - decreased Ca, increased PO4, increased K+

• Acute Tubular Necrosis

Acute Tubular Necrosis

Vasoconstriction & direct damage – inflammatory response, promotes renal tubule epithelial injury; obstructs filtrate

AKI Phases: initiation phase

phase of reduced perfusion or toxicity in which kidney injury is evolving

AKI Phases: extension phase

continued hypoxia following the initial ischemic event and inflammatory response; blood flow returns to proximal tubules

AKI Phases: maintenance phase

cells undergoing repair; can last weeks to months, urine output is lowest

AKI Phases: recovery phase

glomerular function returns but tubules cannot yet concentrate filtrate; return to normal can take 3-12 months

chronic kindye disease is

ESRD – end-stage renal disease

Chronic Kidney Disease (CKD): Diabetic nephropathy

more than 50% of cases; increased glucose leads to basement membrane thickening, increased glomerular permeability; proteinuria, albuminuria

Chronic Kidney Disease (CKD): Hypertensive nephrosclerosis

increased pressure in glomerulus leads to damage of cells, scarring of glomerulus; damage to arterioles – other vessels compensate leading to thickening

Chronic Kidney Disease (CKD): chronic glomerulonephritis

direct injury, antibody deposition & chronic inflammation

CKD Manifestations

retinopathy

peripheral neuropathy

dyspnea on exertion

anorexia

N/V

bone pain

muscle loss

seizures

hypertension

heart failure

amenorrhea

uremic frost

pruitus

CKD and cardiovascular disease

chronic inflammation, hyperlipidemia , hypertension, heart failure

CKD and metabolic acidosis

retain H+ ions

CKD and mineral bone disease

normally, kidneys produce activated Vit D (calcitriol) when Ca falls; end up with hypocalcemia and hyperphosphatemia; high level of bone turnover, fractures

CKD complications

Anemia

hyperkalemia

hypervolemia

uremia

anemia

lack of erythropoietin production; heart remodeling

hyperkalemia

decreased aldosterone secretion, decreased K+ excretion

hypervolemia

decreased excretion of Na+ and H2O

uremia

urea accumulates in bloodstream; N/V, headache fatigue, uremic frost, metallic taste, lethargy, irritability, pruritis