2PF3- Fluid & Electrolyte Imbalances

4 Mechanisms of fluid imbalance

1. Increased capillary hydrostatic pressure

2. Decreased capillary colloidal osmotic pressure

3. Increased interstitial colloidal osmotic pressure

4. Increased tissue hydrostatic pressure

Mechanisms leading to edema

1. Decreased plasma protein production--> decreased capillary oncotic pressure

2. Increased capillary permeability--> loss of intravascular proteins

3. Lymphatic obstruction--> decreased absorption of interstitial fluid

4. Increased capillary hydrostatic pressure--> fluid movement into tissue

Edema vs third spacing

· Edema = interstitial fluid accumulation

· Third-spacing = transcellular fluid accumulation

Transcellular

Small subdivision of the extracellular fluid compartment. Includes various body spaces:

-joint spaces

-pericardial and pleural cavities

-peritoneum

-ocular fluid

Fluid movement in transcellular spaces

-Normally, fluid moves in and out of transcellular spaces using the mechanisms of fluid balance

-When fluid shifts into the transcellular space and cannot be pushed or pulled out of that space, or when there is obstruction to lymphatic flow, fluid becomes trapped in the transcellular space (third spacing)

-This fluid is not readily available for exchange with the rest of the ECF, so is called "non-functional fluid"

Manifestations of edema (brain)

-Signs of increased intracranial pressure

-Mostly associated with infections or trauma (both initiate inflammatory response)

-Skull is an enclosed space with little room for extra fluid... therefore cerebral edema is life threatening

-Signs of increased pressure: headache, LOC, coma, abnormal pupil size/reflexivity, changes in resp. pattern, changes in muscle tone and abnormal posturing

Manifestations of edema (airway)

-Airway swelling also life-threatening

-Frequently due to inflammatory response to allergens or microorganisms

-Swelling may result in difficulty swallowing, anxiety, stridor, possible airway obstruction and asphyxia

Manifestations of edema (lungs)

-Decreased gas exchange and ability of lungs to inflate

-Manifestations may vary according to cause and location of the fluid shift

-Certainly includes dyspnea

-May also experience anxiety, restelessness, diminished breath sounds, and/or crackles

Manifestations of edema (abdomen)

-Ascites is peritoneal third-spacing

-Perhaps due to increased intravascular hydrostatic pressure that results when portal vein is affected by liver cirrhosis

-Perhaps results from significant inflammatory response to something like abdominal tumor or pancreatitis

-Possibe increase in abdominal girth, protruding umbilicus

-May cause abdominal discomfort

-If accumulation of fluid is considerable, also SOB (diaphragm is impeded by fluid)

Manifestations of edema (intestines)

-Third-space loss to intestine

-If intestine is obstructed

Manifestations of edema (peripheral)

-Dependent and pitting edema

-Obstruction of venous blood flow which increases capillary hydrostatic pressure

-Obstruction in lymphatic drainage

-Can occur predominantly in lower extremities in ambulatory patients

-Bedridden patients: can occur in sacral area

What kind of edema is due to salt retention?

Usually pitting edema !! When finger pressed into tissue, fluid shifts and pitting is left. Significant amount of fluid collected

Treatment of edema

- correct the problem

- control the underlying mechanism

- treat the symptoms

- supportive measures

-kidneys will conserve water and sodium, effectively increasing the capillary hydrostatic pressure

-possible diuretic therapy

Treatment of edema (pregnant women with edema in legs/feet)

Elevate legs and avoid standing for long periods of time

Treatment for peripheral edema due to heart disease

Advised to wear supportive stockings to increase interstitial fluid pressure, providing some resistance to the movement of fluid from the capillary to the interstitial space

Treatment of edema (lack of albumin)

May need to treat with albumin infusion

Major regulator of Na+ and H2O balance

Amount of circulating blood volume

Osmoreceptors

Located in the hypothalamus

-Keep track of concentration (osmolality) of the blood

Which electrolyte is predominantly osmotically active particle in the blood?

Na+

Baroreceptors

Located in the blood vessel walls and the kidneys

-Measure the stretch in the vessel walls that is produced by blood volume and pressure

Mechanisms to maintain Na+ and H2O balance

-Thirst

-ADH

-Sympathetic nervous system

-RAAS

-Natriuretic peptides

ADH (Vasopressin)

-Made in the hypothalamus, stored in the posterior pituitary

-Hypothalamus senses low blood volume or increased serum osmolality, sends signals to posterior pituitary to release ADH

-ADH acts on kidney tubules to retain H2O

-Therefore increase in blood volume and decrease serum osmolality

Sympathetic Nervous System (GFR)

-Regulates constriction or relaxation of afferent and efferent arterioles in the kidney, and the amount of glomerular filtrate can be controlled

-If SNS stimualted, afferent arterioles will constrict, limiting amount of blood flow to the kidney, and lowering glomerular filtration pressure

Sympathethic Nervous Sytem (Tubular Reabsorption)

-Sympathetic activity regulates reabsorption of Na+

Sympathetic Nervous System (Renin release)

-Stimulation of SNS results in release of renin

R-A-A-S

Na+ retenetion--> circulating blood volume--> renal perfusion pressure--> juxtaglomerular cells--> renin release--> angiotensinogen to angiotensin I--> angiotensin I to angiotensin II--> aldosterone release --> repeat cycle !

Where are the juxtaglomerular cells located? What do they sense?

Located in kidneys, sense reduced stress in the afferent arterioles, because of reduced blood flow

Where is aldosterone released from? What does it act on?

Adrenals

Works in distal tubule of kidney to promote exchange of Na+ and K+ (Na+ reabsorbed, K+ is lost)

Where does angiotensin II act on?

Acts directly on the kidney tubules to increase Na+ reabsorption

How does Na+ retention increase circulating blood volume

Because Na+ always brings H2O with it!

ANP

Atrial natriuretic peptide

From atrial myocytes

BNP

Brain natriuretic peptide

Mainly from the myocytes of the left ventricle

ANP and BNP

-Respond to increased blood pressure/volume

-Counter-regulatory: excretion of Na+ and water

Who are at the most risk for fluid imbalances?

Infants, elderly, obese, ill patients

Why are infants at high risk for fluid imbalance?

-They have higher % of body water than adults, and more than half their total body water is in the extracellular compartments

-Ingest and excrete a relatively higher amount of water daily compared to adults

-May exchange up to half their ECF! Daily fluid exchange is greater in infants because their high metabolic rate

-Smaller reserve of body fluids than adults

-Inability of immature kidneys to concentrate urine efficiently

-Lose relatively greater fluid loss through skin than adults because of their proportionally greater body surface area

-Both infants and children have immature homeostatic regulating mechanisms, so don't respond as efficiently as adults to small changes in fluid balance

Why are the elderly at high risk for fluid imbalance?

-Aging kidneys--> decrease in glomeruli and decrease in eGFR

-Decrease in ability to concentrate urine

-Slower to respond to Na+ and H2O imbalances, including decreased response to ADH and decreased secretion of aldosterone

-Reduction in total body water

-Thirst sensation decreases with age, therefore fluid intake not necessarily regulated by thirst, but can instead be regulated by food intake (e.g., if an older person isn't eating adequately it is very likely they aren't drinking adequately either)

Why are obese individuals more at risk for fluid imbalances?

Their % of total body water is much less than that of a lean individual, therefore less body water to lose

Why are ill individuals more at risk for fluid imbalances?

-Perhaps due to decreased intake of fluid or increase in fluid losses (fever, vomiting, diarrhea)

-Anyone who experiences an inflammatory response will experience intravascular fluid loss due to increased capillary permeability

-Even if fluid loss is not external (e.g., vomiting), fluid that is not where it's supposed to be can result in dehydration

How to Assess Fluid Balance (main topics)

-Thirst, mucous membranes, turgor, tearing

-Pulse and BP

-Edema

-Weight

-Intake/output; urine concentration

-Neuromuscular signs

Assessing fluid balance (Thirst, mucous mebranes, turgor, tearing)

-An indicator of alterations in body fluid electrolyte balance

-Dry mouth could be due to fluid volume deficit or might simply be a result of mouth breathing

-Skin flattens more slowly in individual with fluid volume deficit (skin turgor). When doing pinch test, it also measure skin elasticity so take this into account

-Obese inflants may maintain skin turgor even when in fluid volume deficit

-In infants, tearing is a reliable indicator of fluid volume, with decreased tearing in those with volume deficit

How to differentiate between dry mouth due to fluid volume deficit vs dry mouth due to mouth breathing

Trick: look in areas where cheeks and gums meet. In mouth breathing these areas remain moist but in fluid volume deficit they are dry

Why is skin turgor not the best indicator of fluid imbalances?

Skin turgor varies considerably with age, nutritional status, race, complexion, etc.

Assessing fluid balance (BP and pulse)

-Tachycardia usually earliest sign of decreased vascular volume

-Alterations in pulse rate, regularity, and volume are present in several types of fluid/electrolyte imbalances

-Take BP reading in standing AND lying positions for more accuracy

Assessing fluid balance (edema)

-Will not become apparent until interstitial fluid volume has increased by at least 2.5 liters

-Check for edema that is generalized, localized, and dependent

Assessing fluid balance (weight)

-Rapid changes in weight reflect changes in body fluid volume

-Generally more accurate than intake and output measurements

-Weigh first thing in the morning--> BEFORE breakfast and AFTER voiding, same scale and same clothing (more accuracy)

Assessing fluid balance (intake/output; urine concentration)

-Should inititate careful intake/output records for any patient with real or potential fluid/electrolyte imbalance

-Urine concentration specific gravity measures ability of the kidneys to concentrate urine

-In fluid volume deficit, body conserves H2O so solutes are excreted in small concentrated urine volume

-High urine levels of unexpected solute such as glucose or albumin will falsely elevate specific gravity readings

Normal urine output (adult) per day and per hour

1000-2000 mL/day

or 40-80 mL/hr

Assessing fluid balance (neuromuscular signs)

-Central and/or peripheral effects

-Headache, anxiety, changes in LOC and twitching

-Some changes can be vague

Disorders of Na+ and H2O Balance (2 main groups)

Proportionate changes in sodium and water (isotonic) and Disproportionate changes in sodium and water

Isotonic fluid deficit

A proportionate change in sodium and water (loss of both!)

Isotonic fluid excess

A proportionate change in sodim and water (gain of both!)

Isotonic Fluid Volume Deficit: Causes

Inadequate intake

-fluids unavailable or withheld

-thirst mechanism impaired

Excessive output

-lost through skin (e.g., wounds/burns)

-lost to third spacing (e.g., peritoneium or intestines)

-lost to the GI tract (single day up to 10 L, but most is reabsorbed... vomiting/diarrhea alter this)

-lost through kidneys (e.g., diseases, drug therapies)

Isotonic fluid volume deficit: manifestations

-Thirst (maybe)

-Decrease in body weight (maybe)

-Decreased urine output; increased SG, osmolality

-Sunken eyes (maybe)

-Loss of skin turgor (maybe)

-Infants: tearing

-Changes in BP and pulse

-Hct, BUN --> become more concentrated

Postural hypotension

Drop in blood pressure upon standing, one of the early signs of fluid deficit. Reflex increase in HR, becomes thready and weak

When tissues lose fluid, what else do they lose?

Resilience

What happens with a severe volume depletion?

Body experiences hypovolemic shock with vascular collapse (hypovolemia can cause renal damage as well)

Isotonic fluid volume deficit: treatment

Straightforward and very important: replace the fluid and treat the cause promptly!

-IV therapy: isontonic losses replaced with isotonic fluids (NS or lactated Ringer's)

-replacing fluids is critical but also just treating the symptoms

Isotonic fluid volume excess: causes

Both extracellular fluid compartments expand, vascular volume, and the interstitial fluid volume

Inadequate elimination

-hypervolemia: body unable to eliminate appropriate amounts of fluid due to poor kidney function. If heart is unable to pump effectively, decreased blood flow to the kidneys will result in fluid retention

Excessive intake

-increased Na+ ingestion results in H2O retention as well, normally kidneys eliminate excess but hypervolemia results if they can't adequately do their job

Why is isotonic fluid excess unusual in healthy individuals?

Because the body's compensatory mechanisms for dealing with excess fluid volume are usually sufficient to restore fluid balance

Isotonic fluid volume excess: manifestations

-weight gain

-edema

-distended neck veins

-bounding pulse

-respiratory symptoms

-decrease in BUN and hematocrit

Isotonic fluid volume excess: treatment

1. stop increasing the volume

-restrict fluid intake

-restrict salt intake

-careful attention to solution for IV fluids and rate of administration

2. start decreasing the volume

-diuretics given to increase Na+ and therefore H2O elimination

3. treat the cause

-e.g. heart failure might be treated with digoxin, which strengthens cardiac contractions and can cause increase kidney perfusion

Hyponatremia

A disproportionate change in sodium and water, loss of sodium or gain of water

*less than 135 mmol/L of Na+

Hypernatremia

A disproportionate change in sodium and water, gain of sodium or loss of water

*more than 145 mmol/L of Na+

Causes of too little ECF sodium

-Either not enough Na+ intake or too much Na+ loss

-Na+ loss related to renal problems (should reserve Na+ through use of aldosterone--> failure to do so may indicate renal impairment or adrenal insufficiency)

-Perhaps loss of Na+ due to diuretic use

-Na+ loss through sweating, vomiting, diarrhea, nasogastric suction (fluid lost in this manner but comparatively more Na+ than H2O)

-Sometimes problem is compounded when client replaces losses with H2O as opposed to electrolyte containing solutions

Causes of too much ECF water

-Osmotic pull and water retention

-e.g., hyperglycemia

-high levels of ADH result in water retention, fairly common in post-operative period and can be made worse if clients are then given electrolyte free IV fluids such as D5W

-sometimes high ADH levels are through inappropriate secretion, mixed up messages in the body (syndrome of inappropriate ADH secretion or SIADH)

-water retention can occur with some medications (e.g., antipsychotics)

Hyponatremia: manifestations

-variable symptoms

-fluid shifts to cells: brain swelling

-inadequate sodium: neuromuscular effects (cramping, weakness, fatigue, tremors)

-labs: decrease serum osmolality

Hyponatremia: treatment

-determine and treat the cause (e.g., medication induced? stop medication)

-decrease the fluid excess (possible fluid or Na+ restriction)

-maybe replace some sodium (if severe.. but should be gradual to avoid huge fluid shifts!)

-monitor carefully (vital signs, neuro status, intake/output, daily weight, lab values)

What is the more common cause of hypernatremia

Too little ECF water is the more common cause compared to too much ECF sodium

Hypernatremia: causes

Too much ECF sodium (too much intake)

Too little ECF water (insufficient intake or abnormal water loss)

-sensible H2O loss through fever, heatstroke, respiratory illness

-significant amount of fluid lost with diarrhea

-Na+ also lost but proportion is less than H2O loss

-osmotic diuresis

-e.g., renal loss of glucose when BG levels are high

Osmotic diuresis

Renal loss of glucose when BG levels are high, therefore at the level of the kidney, loss of particles in the filtrate will cause a related loss of water (which can cause hypernatremia)

Hypernatremia: manifestations

Symptoms depend on why osmolality is increased (e.g., if problem is the increase in Na+, fluid will shift from intracellular compartment to the vasculature because of osmotic pull--> results in shrunken cells)

-shrunken cells (brain cells--> restleness, confused, weak and severe cases stupor, seizure, coma. Skin and mucous membranes)

-neuromuscular excitability such as twitching

-volume depletion--> dry mucous membranes, orthostatic hypertension

-lab values: increased Na+ concentration, increase serum osmolality

-thirst

Hypernatremia: treatment

-decrease the salt

-increase the fluid (oral rehydration via sports drinks, IV solutions)

-correct slowly

When increasing fluids to correct hypernatremia, why is it done slowly/gradually?

Too quickly would cause fluids to shift quickly to brain cells casuing cerebral edema and potentially permanent neurological damage

Potassium

-Major intracellular cation

-Normal concentrations are vital

-Balance is carefully regulated

-Big role in regulating membrane potentials, controlling the excitability of nerve and muscle cells and the contractility of muscles

Normal concentration of potassium IN the cells vs. OUTSIDE the cells... which one do we measure?

In the cells: 140-150 mmol/L

ECF concentration: 3.5-5 mmol/L

We measure ECF for potassium!

Where is potassium primarily lost?

Through renal excretion

Hypokalemia

-Below 3.5 mmol/L

-Too little potassium intake

-Too much potassium output

-Shifts between intracellular and extracellular compartments

How much potassium do adults require daily to balance renal losses?

At least 40 mmol per day

What is the more reasonably common cause of hypokalemia?

Too little potassium intake is more common than too much potassium output

What are common causes for too much potassium output?

-Diuretic use: thiazide and loop diuretics increase loss of K+ in urine

-GI system: excessive loss with vomiting, diarrhea, gastrointestinal suction

-Medications: Insulin promotes movement of K+ into the cells, as do a number of medications such as bronchodilators and decongestants

Hypokalemia: manifestations

-Kidneys

-GI tract

-skeletal muscles

-cardiovascular system (most severe!!)

Manifestations of hypokalemia: GI system

-alters normal peristalsis

-anorexia

-nausea/vomiting may occur

-decreased smooth muscle activity may cause constipation or in severe cases paralytic ileus

Manifestations of hypokalemia: skeletal muscles

Usually gradual in onset, so detecting the problem might take time

At what potassium level do people usually show signs of hypokalemia?

Won't typically show signs until levels fall below 3.0 mmol/L. Signs are usually gradual in onset, so detecting the problem might take time

Manifestations of hypokalemia: cardiovascular system

-Most serious manifestation of hypokalemia, can be life-threatening

-interferes with normal electrical activity AND contractility

-may experience postural hypotension and cardiac arrhythmias

-HR may slow, ECG changes occur

-if excess is severe, ventricular fibrillation and cardiac arrest may occur

Hypokalemia: treatment

-prevention

-replacement: oral (ingest food with high K+ content) and IV

-if severe, may need oral K+ that slowly corrects problem

Hyperkalemia

-too much potassium

-too rapid administration

-too little output

-not common problem but can be serious

-shifts between intracellular and extracellular compartments

Hyperkalemia causes

Renal failure

-decrease in aldosterone--> decrease in Na+ with accompanying decrease in K+

Movement can occur in response to tissue injury

-in periods of acidosis, body tries to compensate for high # of H+ ions by shifting them into the cells. In exchange, K+ ions move out of cells into plasma

At what potassium level are signs of hyperkalemia noticeable?

Often not noticeable until levels exceed 6.0 mmol/L

Hyperkalemia: manifestations

GI: nausea, vomiting, diarrhea

Neuromuscular: excitability, weakness, muscle cramps, parasthesia, may also have normal sensations

Cardiovascular:

Hyperkalemia: treatment

-restrict intake--> salt substitutes

-promote excretion

-discontinue meds that increase K+, such as potassium sparing diuretics

Calcium, Phosphorus, and Magnesium Imbalances

-regulated by vitamin D, parathyroid hormone, and calcitonin

-Neuromuscular and cardiovascular manifestations of imbalances

Normal Ca2+ level

2.1-2.6 mmol/L