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Supporting Increased Cardiac
Output
Fluid and electrolyte imbalances are among the most encountered problems in critically ill clients and are associated with increased morbidity and mortality. Disorders such as severe burns, trauma, sepsis, kidney disease, and heart failure potentially disrupt the finely balanced mechanisms that control fluid and electrolyte balance. Supporting treatments, such as mechanical ventilation and medications, may also affect fluid balance. Monitoring and careful management of electrolytes and fluid balance are integral parts of assessing and caring for a critically ill client. The nurse is caring for a client experiencing hypovolemia. Which action will support an increased preload and improve cardiac output? Administer intravenous bolus 0.9% normal saline
Increased intravenous (IV) fluid administration will increase preload, which will increase cardiac output.
Administration of sodium-free fluids causes cerebral cellular swelling. Dextrose in water causes fluid to shift from the extracellular space into the cells, which caused cerebral cellular swelling and led to seizure activity.
Hormonal Influences on Fluid
Balance
Fluid Homeostasis
The human body strives to consistently achieve fluid balance (homeostasis). There are hundreds of feedback mechanisms in place to ensure homeostasis is maintained. However, fluid and electrolyte imbalances are prevalent in clients with critical illnesses or injuries, because illness disrupts normal homeostatic mechanisms. Many factors contribute to the shifting of fluids and electrolytes among critically ill clients, which compromises their clinical status and adversely affects outcomes. The shifts occur due to underlying chronic diseases and acute conditions, which often occur during the client’s hospitalization. Fluids must be in equilibrium within the intravascular, interstitial, and intracellular spaces. Intracellular fluid volume is relatively stable, whereas intravascular fluid fluctuates in response to fluid intake and loss. Interstitial fluid is the reserve fluid, replacing intravascular and intracellular volume as needed. Kidneys are the primary organ responsible for the absorption, distribution, and excretion of water and its particles. Electrolyte homeostasis is regulated by the kidney and its response to hormones such as aldosterone, anti-diuretic hormone, and natriuretic peptides which work specifically on the renal tubules.
Aldosterone
Aldosterone promotes sodium retention while increasing urinary loss of potassium. Severe hypotension and hypovolemia trigger the release of aldosterone.
Conditions such as diabetes insipidus and syndrome of inappropriate ADH secretion (SIADH) affect the release of this hormone.
Natriuretic Peptides
Natriuretic peptides (atrial natriuretic peptide) are released from the heart in response to chamber stretching and overfilling. Increased renal excretion of sodium, water, and increased glomerular filtration rate occur in response to natriuretic peptide release. Maintaining Fluid Balance The pituitary gland is responsible for the production and release of antidiuretic hormone (ADH). ADH causes renal cells to reabsorb water. This action decreases urine output, concentrating the urine while diluting the blood. In fluid volume deficit, urine specific gravity is increased and in fluid volume overload, urine specific gravity is decreased. A medication given as a replacement for ADH is desmopressin. The posterior pituitary gland releases antidiuretic hormone (ADH), causing renal cells to reabsorb water which decreases urine output, concentrating the urine, and diluting the blood. The normal urine specific gravity is 0.010–0.030. Decreased specific gravity indicates fluid volume overload. Increased specific gravity indicates dehydration.
Desmopressin is a synthetic form of ADH administered intranasally, subcutaneously, or intravenously. Renal Function
Assessing fluid volume status includes:
- Vital signs
- Central venous pressure
- Pulmonary artery pressure
- Breath sounds
- Oxygen saturation
- Skin turgor
- Edema
- Weight
During major illness or injury, normal homeostatic mechanisms are disrupted, often causing fluid alterations.
- Heart failure due to decreased cardiac output can cause fluid overload.
- Renal dysfunction impedes the removal of unneeded fluids.
- Gastrointestinal (GI) loss by vomiting, diarrhea, and gastric suctioning can cause fluid deficit.
- Severe blood loss leads to fluid deficit.
- High fever can cause fluid deficit.
- Lack of antidiuretic hormone (ADH) causes too much fluid excretion. Some treatments lead to fluid alterations.
- Medication use such as diuretics affects fluid balance.
- Nutritional support can lead to fluid retention and/or electrolyte imbalances.
- Mechanical ventilation can lead to fluid retention.
- Surgery can cause fluid retention or fluid loss.
Sodium Imbalances
Sodium imbalances reflect either hyponatremia or hypernatremia and are among the most common electrolyte imbalances encountered in clinical practice. These imbalances are often seen as the most difficult to manage because of their association with water and the variety of
Risk Factors for Fluid Balance
Alterations
Hyponatremia
Hyponatremia typically represents fluid retention. Removal of excess fluid is compromised in many critically ill clients. Heart failure, sepsis, and shock impair glomerular filtration. Some medications as well as pain, nausea, and hypovolemia lead to increased water reabsorption. In addition to renal impairment, inappropriate administration of hypotonic fluid leads to hyponatremia. Hypervolemic hyponatremia often requires restricted sodium and water intake. In clients who are hemodynamically unstable, extracorporeal ultrafiltration may be indicated. Hypernatremia Hypernatremia typically represents fluid depletion and is common in critically ill clients due to water loss from fever, wound drainage, gastrointestinal loss, and diuretic use. Hypovolemic hypernatremia may require the administration of isotonic sodium chloride and/or fluid restrictions. The identification of the cause, and the treatment of the volume loss is essential. Hemodynamic Monitoring
The primary goal of hemodynamic monitoring is the correct assessment of cardiorespiratory pressure and volume variables and their response to fluid regulation, medications, and tissue oxygen demands. Hemodynamic monitoring uses invasive procedures which evaluate oxygenation and perfusion, monitor fluid balance, titrate therapies, and determine illness severity. There are five types of hemodynamic monitoring. Select each tab for details.
Pulmonary Artery (PA) Monitoring
Pulmonary artery (PA) monitoring measures pressure distal to the pulmonary artery, called the pulmonary artery wedge pressure (PAWP). This provides an indirect measurement of left ventricular function. The PA catheter is a multi-lumen, balloon-tipped catheter that is inserted through the venous system into the right side of the heart and the PA. This catheter can be inserted at the bedside from the antecubital vein, external jugular vein, or subclavian vein. Once in the pulmonary artery, the balloon
Pulmonary artery catheter including proximal port, thermistor port, balloon port, distal port, and locations in the heart.
Direct Arterial Blood Pressure Monitoring
Direct arterial monitoring provides continuous arterial blood pressures that are more accurate and reliable than noninvasive blood pressure (BP). Blood sampling for arterial blood gases (ABGs) can be collected through this system without repeated arterial punctures. Arterial hemoglobin oxygen saturation should be 95% to 100%. It is placed in the radial (most common),NOTE: Direct brachial, arterial ormonitoring femoral cannotartery. be used for fluid or medication administration!
Right Atrial Pressure (RAP) Monitoring
Right atrial pressure monitoring measures pressure from the superior or inferior vena cava (CVP) or the right atrium (RA). The pressures from these two areas are essentially equal. RAP is also an
Principles of Invasive Pressure
Monitoring
Bilateral crackles in the lungs, jugular vein distention, and hepatomegaly would indicate hypervolemia and the nurse should anticipate increased CVP and PAWP pressures. Normal central venous pressure (CVP) is 2 to 8 mmHg. Low pressures indicate hypovolemia or extreme vasodilation. High pressures indicate hypervolemia, severe vasoconstriction, pulmonary hypertension, or right ventricular failure. Normal pulmonary arterial wedge pressure (PAWP) is 6 to 12 mmHg. High pressures indicate fluid volume overload. Low pressures indicate volume depletion. Poor skin turgor and dry mucous membranes would indicate hypovolemia and the nurse should anticipate decreased CVP and PAWP pressures. Proper placement of pressure monitoring equipment is essential to obtaining accurate readings. Before the equipment is used, it must be referenced and zeroed. Referencing means placing the transducer so that the zero- reference point is level with the atria of the heart. The phlebostatic axis is used as an external landmark as shown in this image. Zeroing sets a baseline for the system and the point when the monitor reads 0. To zero a transducer, open the reference stopcock to room air and observe the monitor for a reading of 0. This allows the monitor to use atmospheric pressure as a reference for 0. Zeroing is done at setup, immediately after insertion of the line, when the transducer has been disconnected from the pressure
cable, the pressure cables have been disconnected from the monitor, or when the accuracy of measurements is in question.
