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Fluid Volume Overload and Renal Failure - Vocabulary Flashcards

Fluid Volume Overload and Related Electrolyte Imbalances – Comprehensive Notes

  • Overview of fluid volume overload

    • Excess total body water leading to increased preload and perfusion demands on the heart.
    • Vital signs pattern consistent with overload: tachycardia (elevated HR), hypertension (elevated BP), tachypnea (elevated respiratory rate).
    • Temperature may remain normal; external feel may be cool due to interstitial fluid shifts and peripheral vasoconstriction.
    • Objective goal is to identify fluid overload from signs across systems and initiate appropriate management.

  • Respiratory/pulmonary manifestations (pulmonary edema)

    • Shortness of breath (SOB) and orthopnea requiring upright posture to breathe easier.
    • Cyanosis may occur due to hypoxemia.
    • Lung examination: crackles from interstitial and alveolar fluid.
    • Sputum: frothy; pink or blood-tinged indicating blood-tinged froth due to alveolar flooding.
    • Cough: typically wet productive cough.

  • Edema and ascites (third spacing)

    • Weight gain from fluid accumulation; third-spacing edema including ascites.
    • Pitting edema progressing to 4+ indicates severe fluid overload; skin may become stretched and weeping as edema worsens (anasarca).
    • Distinction of ascites from obesity: percussion and physical exam; ascites may show a tympanic (high-pitched) sound indicating ileus/distention.
    • Percussion findings and tests used:
    • Percussion of abdomen helps distinguish ascites vs overweight belly.
    • Fluid wave test: tap one side of abdomen and feel a wave across the abdomen if ascites is present; normal overweight abdomen blocks wave.
    • Temperature of skin over edematous areas may be cooler due to increased fluid between blood and skin reducing heat transfer.
    • JVD (jugular venous distension) assessment is important to gauge central venous pressure and fluid status.
    • Weeping edema and yellow discharge can occur around extremities as skin stretches to max capacity.

  • Neurologic and laboratory changes

    • AMS (altered mental status) and potential cerebral edema from hyponatremia and volume shifts.
    • Seizure risk tied to hyponatremia and electrolyte disturbances; seizures may be linked to hyponatremia rather than volume overload alone.
    • Labs: hyponatremia due to dilution; note that hematocrit/Hgb may be diluted depending on fluid status; urine output tends to be low in overload states.
    • Potassium considerations updated during discussion: hyperkalemia more common with kidney failure; hypokalemia less typical in fluid overload due to kidney failure.
    • Generalized edema termed anasarca when entire body is involved.

  • Fluid management strategies

    • Fluid restriction (and sodium restriction) are primary non-pharmacologic strategies.
    • Sodium restriction is used because water follows sodium; reducing sodium helps control water retention.
    • Hypertonic fluids vs fluid restriction: debate typically favors fixing water balance (water restriction) rather than dialyzing away salt directly in certain contexts.
    • Gold standard pharmacologic approach (acute): loop diuretics (e.g., furosemide/Lasix) to rapidly remove excess fluid.
    • Chronic management: spironolactone (aldosterone antagonist) used for ongoing fluid management and prevention in some settings.
    • Daily weight and strict input/output (I&O) monitoring are essential to track fluid status and diuretic response.
    • Elevate legs and elevate head of bed to facilitate venous return and improve perfusion.
    • Skin integrity: monitor and prevent breakdown due to edema/weeping.

  • Pharmacologic interventions for fluid overload

    • Loop diuretics (Lasix, furosemide) as first-line for acute fluid overload.
    • Spironolactone for chronic control and prevention of fluid overload.
    • If loop diuretics fail to control edema, consider dialysis (see below).
    • Mannitol (osmotic diuretic) as an adjunct to dialysis to mobilize water from third spacing into vasculature.
    • Albumin may be used to enhance dialysis effectiveness in certain cases; clinical response varies between patients and teams.
    • Osmotic diuretic mechanism: pulls fluid from the third space into the vasculature, increasing intravascular volume temporarily to facilitate renal excretion; requires functioning kidneys to actually be excreted.
    • Mannitol administration details:
    • If crystallized at room temperature, warm with warm water in a basin; crystals may form in IV bags as well.
    • Use a filtered needle for drawing up and a filter on IV tubing if giving as IV piggyback.
    • If crystals are visible, re-warm to dissolve.
    • Albumin vs mannitol: both can mobilize fluid into the vasculature to aid dialysis; patient response varies; used judiciously based on clinical scenario.
    • Oxygen therapy as needed to address hypoxemia from pulmonary edema.
    • Physical therapy and activity adjustments: ambulation depends on stability; often activity as tolerated if patient can tolerate, otherwise rest to prevent decompensation.

  • Dialysis as a last-resort therapy

    • Indication when diuretics fail to control fluid overload or when kidney function is severely impaired.
    • Basic dialysis concept (hemodialysis):
    • Access is required (e.g., central line or fistula); blood is drawn out, passes through a dialyzer (with semi-permeable membranes), and returns to the patient.
    • Diasylate (dialysate) on the opposite side of the membrane contains electrolytes at normal levels to pull excess solutes (e.g., potassium) from blood via diffusion and osmosis.
    • The dialysis process relies on concentration gradients to achieve equilibration of electrolytes and fluids across the membrane.
    • Typical dialysis parameters:
    • Flow rate: F = 400\;\frac{mL}{min}
    • Run time: approximately t \approx 3-4\; \text{hours} per session
    • Goal: normalize electrolyte disturbances (e.g., potassium) and remove excess fluid, with daily or scheduled sessions based on patient needs.

  • Potassium management in hyperkalemia

    • Hyperkalemia signs (electrocardiographic and clinical):
    • ECG: tall, peaked T waves; widened QRS complex; prolonged PR interval; U waves may appear; QT interval may appear shortened in some contexts; heart rate may be high or low.
    • Symptoms: muscle cramps, paresthesias, nausea/vomiting (less direct, more often a consequence of metabolic disturbances), possible seizures in severe cases.
    • Chest pain may occur if myocardial ischemia is present, but high potassium alone does not cause a heart attack.
    • Immediate therapies for hyperkalemia (acute management):
    • Insulin with dextrose: Regular insulin IV + 50% dextrose IV (to prevent hypoglycemia); give together (back-to-back) rather than delaying one after the other; insulin drives potassium into cells, dextrose prevents hypoglycemia after insulin.
    • Calcium gluconate: IV calcium to stabilize myocardial membranes; does not lower potassium, but reduces risk of arrhythmias during correction.
    • Potassium binders: Kayexalate (sodium polystyrene sulfonate) or Lokelma (sodium zirconium cyclosilicate) to reduce intestinal potassium absorption/excretion; Lokelma is often preferred due to fewer GI effects, but practice varies.
      • Kayexalate caution: can cause significant diarrhea; less favored now.
      • Lokelma: comes as a powder; requires thorough stirring and prompt administration after mixing; if in NG tube, shake and push rapidly; may require use of a filter in IV tubing if given as IV piggyback.
    • Additional notes on binder choices:
    • Kayexelate (sodium polystyrene sulfonate) vs Lokelma (sodium zirconium cyclosilicate): both bind potassium in the GI tract; Lokelma tends to have a different side-effect profile.
    • Phosphate binders and their interactions with minerals are discussed separately under CKD/phosphate management.

  • Calcium and phosphate management in kidney disease

    • Calcium and phosphate balance is critical in CKD and fluid overload contexts.
    • Vitamin D: essential for calcium absorption; supplementation improves calcium handling.
    • Calcium supplementation: calcium carbonate or calcium acetate (calcium acetate is commonly used as a phosphate binder/adjunct).
    • Phosphate binders (to limit phosphate absorption):
    • Sevelamer (Renagel) – non-calcium binder; binds phosphate in GI tract; does not increase calcium.
    • Lanthanum carbonate (Fosrenol) – another phosphate binder option.
    • Sodium zirconium cyclosilicate (Lokelma) – primarily a potassium binder but discussed here due to overlap in CKD management forums; not a primary phosphate binder.
    • Sevelamer dosing example (hospital practice): 2,000 mg per day in divided doses with meals (e.g., 3 meals/day → ~666 mg per meal).
    • Timing with meals: phosphate binders should be taken with meals to maximize phosphate binding.
    • Phosphorus-rich foods and the role of diet:
    • Dark sodas and highly processed shelf-stable foods are high in phosphorus due to additives; foods like boxed meals (hamburger helpers, Lipton kits, etc.) are phosphorus-rich.
    • Diet should emphasize fresh fruits, vegetables, meats, and seafood; minimize processed foods.
    • Milk is high in both calcium and phosphorus; net effect depends on balance and overall diet.
    • Vitamin D and parathyroid hormone (secondary hyperparathyroidism) management is part of the CKD mineral balance strategy.

  • Dietary and lifestyle considerations for renal failure management

    • Fall prevention: implement fall precautions, use assistive devices as needed, and ensure safe environments.
    • Vitamin D supplementation supports calcium absorption and bone health.
    • Phosphate restriction and binder adherence are critical to prevent hyperphosphatemia and secondary hyperparathyroidism.
    • Sodium restriction helps with fluid management and blood pressure control.
    • Regular monitoring of labs (electrolytes, calcium/phosphorus, vitamin D, PTH) guides therapy.

  • Bedrock principles and safety considerations for vesicants

    • Vesicant medications (e.g., calcium preparations) can cause tissue injury if extravasated.
    • Preferred administration method for vesicants: central venous access when possible; avoid peripheral IVs in small veins for vesicants.
    • If peripheral access is used, ensure large-bore IV (e.g., 18 gauge or larger) and push slowly with dilution and careful monitoring.
    • Central line access reduces risk of extravasation but requires skilled placement and maintenance.
    • Ensure IV patency and blood return before initiating vesicant administration; monitor for signs of infiltration.
    • When administering vesicants, use slow infusion rates, dilute adequately, consider IV pumps when possible, and flush before and after administration.

  • Practical procedural notes for hemodialysis setup and operation (summary)

    • Access planning requires an assessment of options (AV fistula, AV graft, or central venous catheter) with pros/cons for each depending on patient status and duration of therapy.
    • Blood flow and dialysate flow are tuned to achieve effective diffusion and osmosis across the semi-permeable membrane.
    • Dialysate composition is designed to create an appropriate concentration gradient—potassium, calcium, phosphorus, bicarbonate, and other electrolytes in normal physiologic ranges.
    • The goal of dialysis is to correct life-threatening electrolyte disturbances and remove excess fluid in patients with kidney failure or severe overload when diuretics are insufficient.

  • Quick reference: key numerical ranges and dosing references

    • Potassium normal range: K^+ \in [3.5, 5.0]\;\text{mEq/L}
    • Phosphate binder dosing example: 2000\;\text{mg/day} in divided doses with meals; divide across meals (e.g., three meals -> ~667 mg per meal)
    • Dialysis parameters: F_{blood}=400\;\frac{mL}{min}, \quad t\approx 3-4\;\text{hours}
    • Osmotic diuretic mechanism: draws water from third-space fluid into vasculature to facilitate excretion by kidneys when they are functional.
    • Fluid restriction and sodium restriction are foundational non-pharmacologic therapies for fluid overload.

  • Connections to broader principles and clinical relevance

    • Fluid overload management exemplifies the balance between removing excess fluid and maintaining perfusion pressures; aggressive diuresis must be balanced with risk of hypoperfusion and electrolyte shifts.
    • The interplay between acid-base status, electrolyte balance, and neuromuscular excitability underpins signs like tetany and seizure risk in hypocalcemia or hyponatremia scenarios.
    • Dialysis illustrates a practical application of diffusion and osmosis in medicine, converting theoretical physiology into a life-supporting therapy for patients with renal failure or refractory fluid overload.
    • Diet and phosphorus management highlight the connection between nutrition and renal disease outcomes, including bone health and cardiovascular risk.

  • Etiologic and ethical considerations

    • Ethical decisions around escalation to dialysis require assessment of patient stability, prognosis, and goals of care, especially when considering last-resort interventions.
    • Nutritional interventions must balance practicality (cost and access to fresh foods) with clinical goals in order to optimize long-term outcomes.

  • Summary of practical nursing/clinical actions

    • Monitor vital signs closely; watch for signs of decompensation (rapid heart rate, dropping blood pressure, increasing respiratory distress).
    • Implement fluid/sodium restriction plans; ensure patient education on dietary changes and adherence to fluid limits.
    • Initiate diuretic therapy as indicated; monitor daily weights, I&O, and electrolyte trends.
    • Prepare for dialysis escalation when indicated; ensure access planning and multidisciplinary coordination.
    • Manage hyperkalemia promptly with insulin/dextrose, calcium gluconate for cardiac protection, and potassium-binding strategies as appropriate.
    • Use calcium and phosphate management strategies to protect bone health and cardiovascular stability; monitor for signs of hypocalcemia (tetany, Chvostek’s sign, Trousseau’s sign).
    • Maintain safety with vesicant medications, ensuring proper IV access, dilution, and administration technique.