Comprehensive Nursing Study Guide: Fluid Volume Excess, Diuretics, IV Therapy, Shock, and Sodium Imbalances

Fluid Volume Excess (Hypervolemia and Edema)

  • Definition and Pathophysiology:

    • Fluid volume excess occurs when both sodium (Na+\text{Na}^+) and water are retained in the body.

    • It can be caused by fluid overload (excess water and sodium intake) or by an impairment of the physiological mechanisms that maintain homeostasis.

    • The excess fluid retention leads to two main conditions:

      • Hypervolemia: An excess of fluid within the intravascular compartment.

      • Edema: An excess of fluid within the interstitial fluid spaces.

  • Etiology and Underlying Causes:

    • Conditions that impair homeostatic mechanisms and cause simultaneous sodium and water retention include:

      • Heart failure

      • Cirrhosis of the liver

      • Renal failure

      • Adrenal gland disorders

      • Stress conditions that trigger the release of Antidiuretic Hormone (ADH\text{ADH}) and aldosterone

    • Additional causes include:

      • Excessive intake of sodium-containing foods

      • Drugs that cause sodium retention

      • Administration of excessive amounts of sodium-containing intravenous (IV\text{IV}) fluids, such as 0.9% NaCl0.9\%\,\text{NaCl} (normal saline) or Ringer's solution

  • Clinical Manifestations and Complications:

    • Weight Gain: The increase in total body water causes rapid weight gain exceeding 5%5\% of total body weight over a short period.

    • Circulatory Overload Manifestations:

      • Full, bounding pulse

      • Distended neck veins (jugular venous distension) and peripheral veins

      • Elevated Central Venous Pressure (CVP>11−12 cm of water\text{CVP} > 11 - 12\,\text{cm of water})

      • Elevated blood pressure (BP\text{BP}) with a decreased pulse pressure

    • Respiratory System Manifestations:

      • Increased respiratory rate and labored breathing

      • Cough and dyspnea

      • Orthopnea (difficulty breathing when lying supine)

      • Moist crackles (rales) heard upon lung auscultation

      • Pulmonary Edema: A severe complication characterized by excess fluid in the pulmonary interstitial spaces and alveoli

    • Fluid Accumulation and Excretion:

      • Polyuria: Increased urine output if renal excretion function is maintained

      • Ascites: Accumulation of excess fluid in the peritoneal cavity

      • Peripheral Edema: Fluid accumulation in lower extremities or dependent body parts

      • Anasarca: Severe, generalized body edema

    • Subtypes of Overhydration:

      • Isotonic Overhydration: Manifests with liver enlargement and ascites

      • Hypotonic Overhydration: Manifests with polyuria, diarrhea, non-pitting edema, cardiac dysrhythmias, and projectile vomiting

  • Laboratory Findings:

    • Decreased Hematocrit: Values drop below standard normal ranges (normal male: 40−54%40 - 54\%; normal female: 37−49%37 - 49\%) due to plasma dilution.

    • Decreased Blood Urea Nitrogen (BUN): Levels fall below normal limits (10−20 mg/dL10 - 20\,\text{mg/dL}) due to dilution of plasma by excess fluid.

    • Most Common Complications: Heart failure and severe pulmonary edema.

Pharmacological Management: Diuretics

  • General Overview:

    • Diuretics increase the urinary excretion of sodium (Na+\text{Na}^+) and water.

    • They are indicated to enhance renal function and treat vascular fluid overload and tissue edema.

    • Common Side Effects:

      • Orthostatic hypotension

      • Dehydration

      • Electrolyte imbalances

  • Loop Diuretics:

    • Mechanism of Action: Inhibit sodium reabsorption in the thick ascending limb of the loop of Henle.

    • Excretion Profile: Causes an increased excretion of sodium (Na+\text{Na}^+), chloride (Cl−\text{Cl}^-), potassium (K+\text{K}^+), and water.

    • Examples:

      • Furosemide (Lasix)

      • Bumetanide (Bumex)

      • Ethacrynic Acid (Edecrin)

      • Torsemide (Demadex)

  • Thiazide and Thiazide-Like Diuretics:

    • Mechanism of Action: Promote the excretion of sodium, chloride, potassium, and water by decreasing reabsorption in the distal tubule.

    • Examples:

      • Chlorothiazide (Diuril)

      • Hydrochlorothiazide (Hydrodiuril, Oretic)

      • Polythiazide (Renese)

      • Chlortalidone (Hygroton)

      • Trichlormethiazide (Naqua)

  • Potassium-Sparing Diuretics:

    • Mechanism of Action: Promote the excretion of sodium and water while sparing potassium by inhibiting the sodium-potassium (Na+/K+\text{Na}^+/\text{K}^+) exchange mechanism in the distal tubule.

    • Examples:

      • Spironolactone (Aldactone)

      • Amiloride HCl (Midamor)

      • Triamterene (Dyrenium)

  • Client and Family Teaching:

    • Explain that the drug will increase the amount and frequency of urination.

    • Stress that medications must be taken as prescribed even when the patient feels well.

    • Instruct taking the drug in the morning to avoid nocturia and night-time sleep disruption.

    • Advise changing positions slowly (lying to sitting to standing) to prevent orthostatic dizziness.

    • Instruct daily weight monitoring at the same time every day and reporting sudden weight gains or losses.

    • Advise avoiding the use of the salt shaker when eating.

    • If taking a diuretic that increases potassium loss (loop or thiazide), instruct consumption of high-potassium foods such as orange juice and bananas.

Physical Assessment and Nursing Interventions for Fluid Volume Excess

  • System-by-System Physical Assessment:

    • Cardiovascular System: Bounding pulse, increased pulse rate, full peripheral pulses, elevated blood pressure (BP\text{BP}), decreased pulse pressure, elevated central venous pressure (CVP\text{CVP}), and distended neck and hand veins.

    • Respiratory System: Increased respiratory rate, shallow respiration, dyspnea, and moist crackles heard on lung auscultation.

    • Neuromuscular System: Altered level of consciousness (LOC\text{LOC}), headache, visual disturbances, skeletal muscle weakness, and paresthesia.

    • Integumentary System: Pitting edema in dependent areas; skin is pale and cool to touch.

    • Gastrointestinal System: Increased gastrointestinal motility.

  • Nursing Diagnoses and Care Interventions:

    • Nursing Diagnosis: Fluid Volume Excess.

    • Interventions:

      • Administer diuretics as ordered and maintain strict fluid restriction.

      • Monitor fluid status and the physiological effects of fluid volume excess, particularly in patients with cardiac and renal disorders.

      • Assess vital signs, heart sounds, CVP\text{CVP}, and pulse volume of peripheral arteries.

      • Assess for the presence and extent of edema, specifically examining the sacral, back, lower extremities, and periorbital areas:

        • Edema initially affects the lower extremities in ambulatory patients and the sacral region in bedridden patients.

        • Periorbital edema indicates a more generalized systemic edema.

      • Obtain daily weights at the same time of day, using approximately the same clothing and the same scale. Daily weight measurement is one of the most important gauges of fluid balance.

      • Educate the client about a sodium-restricted diet; because excess sodium promotes water retention, restricting sodium reduces water gain.

Intravenous (IV) Therapy and Complications

  • Purposes of IV Therapy:

    • Maintenance of physiological fluid and electrolyte balance

    • Replacement of fluid and electrolyte loss

    • Provision of nutrients

    • Provision of vascular routes for medication administration

  • Complications of IV Therapy:

    • 1. Infiltration:

      • Manifestations: Blanching of skin, swelling, pain at the infusion site, skin cool to touch, and decreased infusion rate.

      • Nursing Interventions: Discontinue IV administration immediately, restart the IV at a new site, and apply warm compresses to increase fluid absorption.

    • 2. Phlebitis:

      • Manifestations: Redness, heat, and swelling at the site, possible pain, and a red line tracking along the course of the vein.

      • Nursing Interventions: Discontinue the IV infusion immediately, restart at a new site, and apply warm compresses to the affected area.

    • 3. Air Embolism:

      • Manifestations: Acute dyspnea, cyanosis, hypotension, loss of consciousness, and tachycardia.

      • Nursing Interventions: Stop the infusion immediately; turn the client onto their left side with the head positioned down (left lateral Trendelenburg position); administer oxygen; notify the physician immediately.

    • 4. Circulatory Overload:

      • Manifestations: Apprehension, shortness of breath, coughing, frothy sputum, pulmonary crackles, engorged neck veins, and elevated blood pressure and pulse rate.

      • Nursing Interventions: Slow down the IV infusion rate; monitor vital signs; notify the physician promptly.

Pathophysiology, Classification, and Management of Shock

  • Definition and Pathophysiology:

    • Shock is an abnormal physiological state in which an imbalance between circulating blood volume and the size of the vascular bed leads to circulatory failure and oxygen/nutrient deprivation of body tissues.

    • Pathophysiological Changes:

      • Hyperventilation leading to respiratory alkalosis

      • Systemic vasoconstriction

      • Compensatory tachycardia

      • Fluid shifts from intracellular fluid (ICF\text{ICF}) to extracellular fluid (ECF\text{ECF}) to maintain circulating blood volume

      • Impaired metabolism: Tissue anoxia forces cells into anaerobic metabolism, causing lactic acid accumulation that results in metabolic acidosis

      • Impaired organ function:

        • Kidneys: Decreased renal perfusion can result in acute renal failure

        • Lungs: Ischemia can lead to acute respiratory distress syndrome (ARDS\text{ARDS})

  • Classifications of Shock:

    • Hypovolemic Shock: Caused by a direct decrease in circulating blood volume.

      • Causes: Whole blood loss, plasma loss (such as in burns), or fluid loss (excessive vomiting or diarrhea).

    • Cardiogenic Shock: Caused by failure of the heart muscle to pump properly.

      • Causes: Myocardial infarction (MI\text{MI}), congestive heart failure (CHF\text{CHF}), pericardial tamponade (accumulation of blood or fluid in the pericardium that prevents adequate ventricular filling), or tension pneumothorax (air enters the pleural space with each inspiration but cannot escape, leading to increased intrathoracic pressure).

    • Septic Shock: Caused by severe systemic infection and systemic toxin release.

      • Predisposing Factors: Development of antibiotic-resistant organisms, immunosuppression, and advanced age.

      • Causes: Release of bacterial toxins that act directly on blood vessels to produce massive vasodilation and vascular pooling of blood; results most frequently from gram-negative septicemia.

    • Neurogenic Shock: Caused by failure of arteriolar resistance/tone leading to massive vasodilation and pooling of blood.

      • Causes: Interruption of sympathetic nervous impulses due to exposure to unpleasant circumstances, extreme pain, severe head injury, or vasomotor depression.

    • Anaphylactic Shock: Caused by massive vasodilation resulting from a severe allergic reaction that triggers the release of histamine and related vasoactive substances.

      • Causes: Allergic reactions to insect venom, specific medications, or dyes used in radiological studies.

  • Drugs Used to Treat Shock:

    • Dopamine (Intropin):

      • Low Dosage: Dilates renal and mesenteric arteries, which increases perfusion to the kidneys.

      • High Dosage: Increases myocardial contractility and induces systemic vasoconstriction.

    • Dobutamine (Dobutrex): Increases myocardial contractility and acts as a vasodilator.

    • Norepinephrine (Levophed): Improves cardiac contractility and cardiac output; acts as a potent vasoconstrictor.

    • Isoproterenol (Isuprel): Increases myocardial contractility and decreases peripheral resistance by dilating the peripheral vascular bed.

    • Antibiotics: Administered to eliminate infectious agents related to septic shock.

    • Corticosteroids:

      • Indication: Used especially in septic shock to protect cell membranes and decrease the inflammatory response to stress.

      • Commonly Used Agents: Cortisone, Hydrocortisone, Prednisone, Dexamethasone (Decadron).

      • Common Side Effects: Salt and water retention, sweating, and increased appetite.

    • Digitalis Preparation (Cardiac Glycosides):

      • Digoxin (Lanoxin): Improves myocardial contractility by increasing the amount of calcium available for contraction; increases stroke volume and cardiac output; possesses electrophysiological properties that slow conduction, leading to a decrease in heart rate and reduced myocardial oxygen consumption.

Sodium Imbalances: Hyponatremia and Hypernatremia

  • Physiology and Normal Regulation of Sodium:

    • Sodium (Na+\text{Na}^+) is the most plentiful electrolyte in extracellular fluid (ECF\text{ECF}).

    • Normal serum sodium range: 135−145 mEq/L135 - 145\,\text{mEq/L}.

    • Serves as the primary regulator of fluid volume, osmolality, and ECF distribution; plays an essential role in neuromuscular activity.

    • Normal Sodium Balance:

      • Dietary intake is the primary sodium source; an intake of 500 mg/day500\,\text{mg/day} is sufficient to meet baseline physiological needs.

      • Prescription drugs represent additional sodium sources.

      • Excreted primarily by the kidneys, with small amounts excreted through the skin and gastrointestinal tract.

      • The kidney is the primary regulator of sodium balance, excreting or conserving sodium in response to vascular volume changes.

    • Mechanism during Blood Volume Decrease:

      • Activation of the Renin-Angiotensin-Aldosterone System (RAAS\text{RAAS}).

      • Release of Antidiuretic Hormone (ADH\text{ADH}) from the posterior pituitary gland.

      • ADH\text{ADH} promotes sodium and water reabsorption in distal renal tubules, reducing urine output and expanding blood volume.

    • Mechanism during Blood Volume Expansion:

      • Glomerular Filtration Rate (GFR\text{GFR}) increases, allowing more water and sodium to be filtered and excreted.

      • Atrial Natriuretic Peptide (ANP\text{ANP}) is released by cells in the cardiac atria, increasing renal sodium excretion.

      • ADH\text{ADH} release from the pituitary gland is inhibited, making distal tubules relatively impermeable to water and sodium, increasing urine excretion.

  • Hyponatremia:

    • Definition: Serum sodium level below 135 mEq/L135\,\text{mEq/L}. Hypoosmolar ECF draws water into body cells, causing cellular swelling.

    • Causes:

      • 1. Increased Sodium Excretion: Excessive diaphoresis, high-ceiling loop diuretics, GI wound drainage, decreased aldosterone secretion, renal disease.

      • 2. Inadequate Sodium Intake: Low-salt diet, NPO (nothing by mouth) status.

      • 3. Dilution of Serum Sodium: Excessive ingestion of hypotonic fluids, renal failure, Syndrome of Inappropriate Antidiuretic Hormone (SIADH\text{SIADH}), hyperglycemia, congestive heart failure (CHF\text{CHF}).

    • Assessment Manifestations by System:

      • Cardiovascular: Normovolemic = rapid pulse rate, normal BP; Hypovolemic = thready, weak, rapid pulse rate, hypotension, flat neck veins, normal or low CVP\text{CVP}; Hypervolemic = rapid, bounding pulse, normal or elevated BP, normal or elevated CVP\text{CVP}.

      • Respiratory: Signs of pulmonary edema (rapid, shallow respirations, moist crackles/rales); shallow ineffective respirations due to skeletal muscle weakness.

      • Neuromuscular: Generalized skeletal muscle weakness worst in lower extremities, diminished deep tendon reflexes (DTRs\text{DTRs}).

      • Cerebral Function: Headache, personality changes.

      • Gastrointestinal: Increased motility, hyperactive bowel sounds, nausea, abdominal cramping, diarrhea.

      • Renal: Increased urinary output, decreased urine specific gravity.

    • Diagnostic Findings:

      • Serum sodium: <135 mEq/L< 135\,\text{mEq/L}

      • Serum osmolality: <275 mOsm/kg< 275\,\text{mOsm/kg}

    • Medical and Dietary Management:

      • Administer isotonic IV solutions (0.9% NaCl0.9\%\,\text{NaCl}) when both water and sodium are lost.

      • Administer loop diuretics for hyponatremia with normal or excess ECF volume to promote isotonic diuresis without worsening sodium loss. Avoid thiazide diuretics because they cause greater sodium loss relative to water loss.

      • For mild hyponatremia, restrict fluids to reduce ECF volume and increase dietary intake of high-sodium foods.

      • High-Sodium Foods: Table salt, milk, butter, ketchup, soy sauce, mustard, bacon, cured pork, canned food, processed food, cottage cheese, snack foods.

    • Nursing Monitoring:

      • Monitor mental status and orientation continuously: serum sodium levels of 115−120 mEq/L115 - 120\,\text{mEq/L} cause headache, lethargy, and decreased orientation; levels of 110−115 mEq/L110 - 115\,\text{mEq/L} can cause seizures and coma.

      • Assess muscle strength, tone, and deep tendon reflexes; increasing weakness and decreasing DTRs\text{DTRs} signal worsening hyponatremia.

  • Hypernatremia:

    • Definition: Serum sodium level above 145 mEq/L145\,\text{mEq/L}. Occurs when sodium is gained in excess of water or water is lost in excess of sodium. Can accompany fluid volume deficit or excess. High ECF sodium levels draw water out of body cells, causing cellular shrinkage.

    • Causes:

      • 1. Decreased Sodium Excretion: Corticosteroid therapy, Cushing's syndrome, renal failure, hyperaldosteronism.

      • 2. Increased Sodium Intake: Excessive oral sodium ingestion, excessive administration of sodium-containing IV fluids.

      • 3. Decreased Water Intake: NPO status.

      • 4. Increased Water Loss: Elevated metabolic rate, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, dehydration.

    • Regulatory Protective Mechanisms:

      • Excess ECF sodium stimulates posterior pituitary ADH\text{ADH} release, increasing renal water retention.

      • The hypothalamic thirst mechanism is stimulated to increase oral fluid intake. Both mechanisms expand extracellular water to dilute excess sodium back toward normal limits.

    • Assessment Manifestations by System:

      • Cardiovascular: Decreased myocardial contractility and diminished cardiac output; heart rate and blood pressure vary depending on overall vascular volume.

      • Respiratory: Pulmonary edema present if accompanied by hypervolemia.

      • Neuromuscular: Early stage = spontaneous muscle twitches, irregular muscle contractions; Late stage = skeletal muscle weakness, diminished or absent deep tendon reflexes.

      • Central Nervous System (CNS): Altered cerebral function is the cardinal manifestation. Normovolemia/Hypovolemia = agitation, confusion, seizures; Hypervolemia = lethargy, stupor, coma.

      • Renal System: Increased urine specific gravity, decreased urinary output.

      • Integumentary System: Dry, flaky skin; edema present or absent depending on volume changes.

    • Diagnostic Findings:

      • Serum sodium: >145 mEq/L> 145\,\text{mEq/L}

      • Serum osmolality: >295 mOsm/kg> 295\,\text{mOsm/kg}

    • Medical Management:

      • Administer hypotonic IV solutions to correct water deficits.

      • Administer diuretics to promote renal sodium excretion.





Fluid Volume Excess (Hypervolemia and Edema)

Definition and Pathophysiology:

Fluid volume excess (FVE) occurs when both sodium (Na+Na+) and water are retained in the extracellular fluid in isotonic proportions.

It results from either excessive fluid/sodium intake or an impairment of normal physiological homeostatic mechanisms.

The excess fluid retention manifests in two main fluid compartments:

Hypervolemia:  Expansion of intravascular fluid volume within the vascular system.

Edema:  Accumulation of excess fluid within interstitial fluid spaces.

Etiology and Underlying Causes:

Pathological Conditions Impairing Homeostasis:

Heart Failure:  Decreased cardiac output leads to compensatory activation of fluid-retaining mechanisms.

Cirrhosis of the Liver:  Impaired hepatic function and portal hypertension result in fluid sequestration and secondary aldosterone elevation.

Renal Failure:  Impaired glomerular filtration and tubular excretion reduce sodium and water excretion.

Adrenal Gland Disorders:  Excessive secretion of aldosterone increases distal tubular renal sodium reabsorption.

Stress Responses:  Trigger physiological release of Antidiuretic Hormone (ADHADH) and aldosterone.

Iatrogenic and Dietary Factors:

Ingestion of foods high in sodium.

Medications promoting sodium retention (e.g., corticosteroids).

Excessive or rapid infusion of sodium-containing intravenous (IVIV) solutions (e.g., 0.9% NaCl0.9%NaCl normal saline or Ringer's solution).

Clinical Manifestations and Complications:

Weight Changes:  Rapid body weight gain exceeding 5%5% of baseline total body weight over a short duration.

Circulatory Overload Manifestations:

Full, bounding peripheral and central pulses.

Distended neck veins (jugular venous distension) and engorged peripheral veins.

Elevated Central Venous Pressure (CVP>11−12 cm of waterCVP>11−12cm of water).

Elevated systemic blood pressure (BPBP) accompanied by a decreased/narrowed pulse pressure.

Respiratory System Manifestations:

Increased respiratory rate (tachypnea) and labored, shallow breathing.

Dyspnea and persistent cough.

Orthopnea (difficulty breathing when lying supine).

Auscultation of moist crackles (rales) in lung fields.

Pulmonary Edema:  A severe complication characterized by excess fluid shifting into pulmonary interstitial spaces and alveoli.

Fluid Distribution and Excretion:

Polyuria:  Increased urine output if renal excretion function is preserved.

Ascites:  Accumulation of excess fluid within the peritoneal cavity.

Peripheral Edema:  Fluid accumulation in lower extremities or dependent body parts.

Anasarca:  Severe, generalized body edema.

Subtypes of Overhydration:

Isotonic Overhydration:  Involves proportional sodium and water expansion; characteristically manifests with liver enlargement (hepatomegaly) and ascites.

Hypotonic Overhydration:  Involves water gain exceeding sodium gain; manifests with polyuria, diarrhea, non-pitting edema, cardiac dysrhythmias, and projectile vomiting.

Laboratory Findings:

Decreased Hematocrit:  Values drop below standard normal ranges (normal male: 40−54%40−54%; normal female: 37−49%37−49%) due to plasma dilution.

Decreased Blood Urea Nitrogen (BUN):  Levels fall below normal limits (10−20 mg/dL10−20mg/dL) due to dilution of plasma by excess fluid.

Primary Complications:  Acute heart failure and severe pulmonary edema.

Pharmacological Management: Diuretics

General Overview:

Diuretics increase the urinary excretion of sodium (Na+Na+) and water.

Indications: Enhance renal function, treat vascular circulatory overload, and relieve tissue edema.

Common Side Effects:

Orthostatic (postural) hypotension.

Dehydration.

Electrolyte imbalances.

Loop Diuretics:

Mechanism of Action:  Inhibit sodium, potassium, and chloride reabsorption in the thick ascending limb of the loop of Henle.

Excretion Profile:  Causes an increased renal excretion of sodium (Na+Na+), chloride (Cl−Cl−), potassium (K+K+), and water.

Representative Examples:

Furosemide (Lasix)

Bumetanide (Bumex)

Ethacrynic Acid (Edecrin)

Torsemide (Demadex)

Thiazide and Thiazide-Like Diuretics:

Mechanism of Action:  Promote excretion of sodium, chloride, potassium, and water by decreasing reabsorption in the distal tubule.

Representative Examples:

Chlorothiazide (Diuril)

Hydrochlorothiazide (Hydrodiuril, Oretic)

Polythiazide (Renese)

Chlortalidone (Hygroton)

Trichlormethiazide (Naqua)

Potassium-Sparing Diuretics:

Mechanism of Action:  Promote excretion of sodium and water while sparing potassium by inhibiting the sodium-potassium (Na+/K+Na+/K+) exchange mechanism in the distal tubule.

Representative Examples:

Spironolactone (Aldactone)

Amiloride HCl (Midamor)

Triamterene (Dyrenium)

Client and Family Teaching:

Explain that diuretic therapy increases the amount and frequency of urination.

Stress that medications must be taken as prescribed even when the patient feels well.

Instruct taking the drug in the morning to avoid nocturia and night-time sleep disruption.

Advise changing positions slowly (lying to sitting to standing) to prevent orthostatic dizziness.

Instruct daily weight monitoring at the same time every day, on the same scale; report sudden weight gains or losses.

Advise avoiding the use of the salt shaker when eating.

If taking a diuretic that increases potassium loss (loop or thiazide), instruct consumption of high-potassium foods such as orange juice and bananas.

Physical Assessment and Nursing Interventions for Fluid Volume Excess

System-by-System Physical Assessment:

Cardiovascular System:  Bounding pulse, increased pulse rate, full peripheral pulses, elevated blood pressure (BPBP), decreased pulse pressure, elevated central venous pressure (CVPCVP), and distended neck and hand veins.

Respiratory System:  Increased respiratory rate, shallow respiration, dyspnea, and moist crackles heard on lung auscultation.

Neuromuscular System:  Altered level of consciousness (LOCLOC), headache, visual disturbances, skeletal muscle weakness, and paresthesia.

Integumentary System:  Pitting edema in dependent areas; skin is pale and cool to touch.

Gastrointestinal System:  Increased gastrointestinal motility.

Nursing Diagnoses and Care Interventions:

Nursing Diagnosis:  Fluid Volume Excess.

Interventions:

Administer diuretics as ordered and maintain strict fluid restriction.

Monitor fluid status and physiological effects of fluid volume excess, particularly in patients with cardiac and renal disorders.

Assess vital signs, heart sounds, CVPCVP, and pulse volume of peripheral arteries.

Assess for presence and extent of edema, specifically examining sacral, back, lower extremity, and periorbital areas:

Edema initially affects lower extremities in ambulatory patients and the sacral region in bedridden patients.

Periorbital edema indicates a more generalized systemic edema.

Obtain daily weights at the same time of day, using approximately the same clothing and the same scale.

Educate the client about a sodium-restricted diet; restricting sodium reduces osmotic water gain.

Intravenous (IV) Therapy and Complications

Purposes of IV Therapy:

Maintenance of physiological fluid and electrolyte balance.

Replacement of acute or ongoing fluid and electrolyte loss.

Provision of metabolic nutrients.

Provision of vascular routes for medication administration.

Complications of IV Therapy:

  1. Infiltration:

Manifestations:  Blanching of skin, swelling, pain at infusion site, cool skin to touch, and decreased infusion rate.

Nursing Interventions:  Discontinue IV administration immediately, restart IV at a new site, and apply warm compresses to increase fluid absorption.

  1. Phlebitis:

Manifestations:  Redness, heat, and swelling at site, pain, and a red line tracking along the course of the vein.

Nursing Interventions:  Discontinue IV infusion immediately, restart at a new site, and apply warm compresses to the affected area.

  1. Air Embolism:

Manifestations:  Acute dyspnea, cyanosis, hypotension, loss of consciousness, and tachycardia.

Nursing Interventions:  Stop infusion immediately; turn client onto left side with head positioned down (left lateral Trendelenburg position); administer oxygen; notify physician immediately.

  1. Circulatory Overload:

Manifestations:  Apprehension, shortness of breath, coughing, frothy sputum, pulmonary crackles, engorged neck veins, elevated blood pressure, and pulse rate.

Nursing Interventions:  Slow down IV infusion rate; monitor vital signs; notify physician promptly.

Pathophysiology, Classification, and Management of Shock

Definition and Pathophysiology:

Shock is an abnormal physiological state in which an imbalance between circulating blood volume and the size of the vascular bed leads to circulatory failure and oxygen/nutrient deprivation of body tissues.

Pathophysiological Changes:

Hyperventilation leading to respiratory alkalosis.

Systemic vasoconstriction and compensatory tachycardia.

Fluid shifts from intracellular fluid (ICFICF) to extracellular fluid (ECFECF) to maintain circulating blood volume.

Impaired metabolism: Tissue anoxia forces cells into anaerobic metabolism, causing lactic acid accumulation that results in metabolic acidosis.

Impaired organ function:

Kidneys:  Decreased renal perfusion can result in acute renal failure.

Lungs:  Ischemia can lead to acute respiratory distress syndrome (ARDSARDS).

Classifications of Shock:

Hypovolemic Shock:  Caused by a direct decrease in circulating blood volume.

Causes:  Whole blood loss, plasma loss (such as in burns), or fluid loss (excessive vomiting or diarrhea).

Cardiogenic Shock:  Caused by failure of the heart muscle to pump properly.

Causes:  Myocardial infarction (MIMI), congestive heart failure (CHFCHF), pericardial tamponade (accumulation of blood or fluid in pericardium preventing ventricular filling), or tension pneumothorax (trapped air in pleural space increasing intrathoracic pressure).

Septic Shock:  Caused by severe systemic infection and systemic toxin release.

Predisposing Factors:  Development of antibiotic-resistant organisms, immunosuppression, and advanced age.

Causes:  Release of bacterial toxins acting on blood vessels to produce massive vasodilation and vascular pooling; results most frequently from gram-negative septicemia.

Neurogenic Shock:  Caused by failure of arteriolar resistance/tone leading to massive vasodilation and pooling of blood.

Causes:  Interruption of sympathetic nervous impulses due to exposure to unpleasant circumstances, extreme pain, severe head injury, or vasomotor depression.

Anaphylactic Shock:  Caused by massive vasodilation resulting from a severe allergic reaction triggering histamine release.

Causes:  Allergic reactions to insect venom, specific medications, or dyes used in radiological studies.

Drugs Used to Treat Shock:

Dopamine (Intropin):

Low Dosage:  Dilates renal and mesenteric arteries, increasing perfusion to kidneys.

High Dosage:  Increases myocardial contractility and induces systemic vasoconstriction.

Dobutamine (Dobutrex):  Increases myocardial contractility and acts as a vasodilator.

Norepinephrine (Levophed):  Improves cardiac contractility and cardiac output; acts as a potent vasoconstrictor.

Isoproterenol (Isuprel):  Increases myocardial contractility and decreases peripheral resistance by dilating the peripheral vascular bed.

Antibiotics:  Administered to eliminate infectious agents related to septic shock.

Corticosteroids:

Indication:  Used especially in septic shock to protect cell membranes and decrease the inflammatory response to stress.

Commonly Used Agents:  Cortisone, Hydrocortisone, Prednisone, Dexamethasone (Decadron).

Common Side Effects:  Salt and water retention, sweating, and increased appetite.

Digitalis Preparation (Cardiac Glycosides):

Digoxin (Lanoxin):  Improves myocardial contractility by increasing calcium availability; increases stroke volume and cardiac output; slows conduction leading to decreased heart rate and reduced myocardial oxygen consumption.

Sodium Imbalances: Hyponatremia and Hypernatremia

Physiology and Normal Regulation of Sodium:

Sodium (Na+Na+) is the most plentiful electrolyte in extracellular fluid (ECFECF).

Normal serum sodium range: 135−145 mEq/L135−145mEq/L.

Serves as the primary regulator of fluid volume, osmolality, and ECF distribution; plays an essential role in neuromuscular activity.

Normal Sodium Balance:

Dietary intake is the primary sodium source; an intake of 500 mg/day500mg/day is sufficient to meet baseline physiological needs.

Prescription drugs represent additional sodium sources.

Excreted primarily by kidneys, with small amounts excreted through skin and GI tract.

The kidney is the primary regulator of sodium balance, excreting or conserving sodium in response to vascular volume changes.

Mechanism during Blood Volume Decrease:

Activation of the Renin-Angiotensin-Aldosterone System (RAASRAAS).

Release of Antidiuretic Hormone (ADHADH) from posterior pituitary gland.

ADHADH promotes sodium and water reabsorption in distal renal tubules, reducing urine output and expanding blood volume.

Mechanism during Blood Volume Expansion:

Glomerular Filtration Rate (GFRGFR) increases, allowing more water and sodium to be filtered and excreted.

Atrial Natriuretic Peptide (ANPANP) is released by cardiac atria, increasing renal sodium excretion.

ADHADH release is inhibited, making distal tubules relatively impermeable to water and sodium, increasing urine excretion.

Hyponatremia:

Definition:  Serum sodium level below 135 mEq/L135mEq/L. Hypoosmolar ECF draws water into body cells, causing cellular swelling.

Causes:

  1. Increased Sodium Excretion:  Excessive diaphoresis, high-ceiling loop diuretics, GI wound drainage, decreased aldosterone secretion, renal disease.

  2. Inadequate Sodium Intake:  Low-salt diet, NPO (nothing by mouth) status.

  3. Dilution of Serum Sodium:  Excessive ingestion of hypotonic fluids, renal failure, Syndrome of Inappropriate Antidiuretic Hormone (SIADHSIADH), hyperglycemia, congestive heart failure (CHFCHF).

Assessment Manifestations by System:

Cardiovascular:  Normovolemic = rapid pulse rate, normal BP; Hypovolemic = thready, weak, rapid pulse rate, hypotension, flat neck veins, normal or low CVPCVP; Hypervolemic = rapid, bounding pulse, normal or elevated BP, normal or elevated CVPCVP.

Respiratory:  Signs of pulmonary edema (rapid, shallow respirations, moist crackles/rales); shallow ineffective respirations due to muscle weakness.

Neuromuscular:  Generalized skeletal muscle weakness worst in lower extremities, diminished deep tendon reflexes (DTRsDTRs).

Cerebral Function:  Headache, personality changes.

Gastrointestinal:  Increased motility, hyperactive bowel sounds, nausea, abdominal cramping, diarrhea.

Renal:  Increased urinary output, decreased urine specific gravity.

Diagnostic Findings:

Serum sodium: \nSerum osmolality: Medical and Dietary Management:

Administer isotonic IV solutions (0.9% NaCl0.9%NaCl) when both water and sodium are lost.

Administer loop diuretics for hyponatremia with normal or excess ECF volume to promote isotonic diuresis without worsening sodium loss. Avoid thiazide diuretics because they cause greater sodium loss relative to water loss.

For mild hyponatremia, restrict fluids to reduce ECF volume and increase dietary intake of high-sodium foods (table salt, milk, butter, ketchup, soy sauce, mustard, bacon, cured pork, canned food, processed food, cottage cheese, snack foods).

Nursing Monitoring:

Monitor mental status and orientation continuously: serum sodium levels of 115−120 mEq/L115−120mEq/L cause headache, lethargy, and decreased orientation; levels of 110−115 mEq/L110−115mEq/L can cause seizures and coma.

Assess muscle strength, tone, and deep tendon reflexes; increasing weakness and decreasing DTRsDTRs signal worsening hyponatremia.

Hypernatremia:

Definition:  Serum sodium level above 145 mEq/L145mEq/L. Occurs when sodium is gained in excess of water or water is lost in excess of sodium. Can accompany fluid volume deficit or excess. High ECF sodium levels draw water out of body cells, causing cellular shrinkage.

Causes:

  1. Decreased Sodium Excretion:  Corticosteroid therapy, Cushing's syndrome, renal failure, hyperaldosteronism.

  2. Increased Sodium Intake:  Excessive oral sodium ingestion, excessive administration of sodium-containing IV fluids.

  3. Decreased Water Intake:  NPO status.

  4. Increased Water Loss:  Elevated metabolic rate, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, dehydration.

Regulatory Protective Mechanisms:

Excess ECF sodium stimulates posterior pituitary ADHADH release, increasing renal water retention.

Hypothalamic thirst mechanism is stimulated to increase oral fluid intake, diluting sodium back toward normal limits.

Assessment Manifestations by System:

Cardiovascular:  Decreased myocardial contractility and diminished cardiac output; heart rate and blood pressure vary depending on overall vascular volume.

Respiratory:  Pulmonary edema present if accompanied by hypervolemia.

Neuromuscular:  Early stage = spontaneous muscle twitches, irregular muscle contractions; Late stage = skeletal muscle weakness, diminished or absent deep tendon reflexes.

Central Nervous System (CNS):  Altered cerebral function is the cardinal manifestation. Normovolemia/Hypovolemia = agitation, confusion, seizures; Hypervolemia = lethargy, stupor, coma.

Renal System:  Increased urine specific gravity, decreased urinary output.

Integumentary System:  Dry, flaky skin; edema present or absent depending on volume changes.

Diagnostic Findings:

Serum sodium: >145 mEq/L>145mEq/L

Serum osmolality: >295 mOsm/kg>295mOsm/kg

Medical Management:

Administer hypotonic IV solutions to correct water deficits.

Administer diuretics to promote renal sodium excretion.