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NR341 WEEK 4
Introduction to Nursing Care: Complex Fluid Balance Alterations 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.
- 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 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.
HORMONAL INFLUENCES ON FLUID BALANCE
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 (HOLDS SODIUM)
Aldosterone promotes sodium retention while increasing urinary loss of potassium. Severe hypotension and hypovolemia trigger the release of aldosterone.
Antidiuretic Hormone (ADH) (HOLDS WATER)
Antidiuretic hormone (ADH) triggers the renal tubules to reabsorb water and return it to the intravascular space. Hypovolemia and increased blood osmolarity cause ADH to be released. Conditions such as diabetes insipidus and syndrome of inappropriate ADH secretion (SIADH) affect the release of this hormone.
Natriuretic Peptides (EXCRETE SODIUM AND WATER)
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. RENAL FUNCTION Optimal kidney function is essential to maintain homeostasis. It is essential to assess kidney function in clients with fluid and electrolyte imbalances. Important laboratory tests that reflect kidney function include:
- albumin
- calcium
- creatinine
- chloride
- glucose
HEMODYNAMIC MONITORING
Noninvasive Blood pressure cuff Capnography Pulse oximeter EKG Invasive Catheter attached to monitoring system that has transducer to display electrical signals as the blood flows through the catheter. *Monitor for cues of worsening condition – oxygenation & fluid. Will use chest xray to confirm placement PRINCIPLES OF INVASIVE PRESSURE MONITORING Reference and zeroed Landmark: Phlebostatic axis Open stopcock Zeroing:
- Setup
- After insertion
- Any disconnection
- Questionable readings
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.
- The catheter, pressure tubing, flush system, and transducer are disposable. NURSING ROLE DURING HEMODYNAMIC MONITORING Client/family education Consent forms Equipment setup Assist with insertion Observe and assess tracing Save practices Observe for complications Occlusive sterile dressing Assess the client (IMPORTANT) COMPLICATIONS OF HEMODYNAMIC MONITORING Complications of Art lines Hemorrhage Infection Thrombus formation Neurovascular impairment Prevention Secure connections
Electrolytes Signs of bleeding Infection Fluid overload may require the use of extracorporeal therapies, such as continuous renal replacement therapy (CRRT), to manage hemodynamic instability and multiple organ dysfunction in critically ill clients. CRRT provides a slow, continuous form of fluid removal, resulting in greater hemodynamic stability and improved fluid balance control CRRT is used as an emergency treatment for clients with fluid overload, blood toxins, symptomatic uremia, hyperkalemia, and metabolic or hemodynamic instability. It is contraindicated in clients with severe hyperkalemia or pericarditis that need rapid treatment. Before using continuous renal replacement therapy (CRRT), consideration of available resources, nursing expertise, and client hemodynamic stability must be reviewed. Nursing care during CRRT includes:
- prepare for CRRT by collecting baseline assessment data
- monitor the hourly output from CRRT and assess fluid volume status
- administer fluid replacement based on hourly fluid balance
- assess for neurologic changes
- assess electrolyte and acid-base balance regularly
- assess temperature and for signs of bleeding
- assess for signs of infection
- assess coagulation status
- maintain patency of the circuit INTRODUCTION TO NURSING CARE: SHOCK 4 Types Hypovolemic shock – decreased circulating blood volume Cardiogenic shock – cardiac failure Obstructive shock – blockage of blood flow outside heart
Distributive shock – excessive dilation of venules/arterioles, anaphylactic, septic, neurogenic
Shock is a state of inadequate tissue perfusion leading to impaired cellular
function and organ failure. Any condition that compromises oxygen delivery to organs and tissues can lead to shock. There are four main categories:
- cardiogenic
- hypovolemic
- distribution
- obstructive Shock, of any cause, is rapidly progressing and life-threatening. The cause, initial presentation, and management may vary according to the type of shock. Nurses must be able to recognize early signs to improve client outcomes.
Cardiogenic shock occurs when the heart fails to pump effectively due to a
cardiac cause. Dobutamine increases contractility, allowing the heart to pump more effectively.
In obstructive shock , the obstruction causes a high afterload. Medications
will not resolve the problem.
In hypovolemic shock , fluid replacement as well as reducing fluid loss are
the main goals.
In distributive shock , the afterload has already decreased.
Initial stage of shock there is no visible change in physiologic parameters because changes are occurring at the cellular level. Oxygen is shunted to vital organs. The heart rate may be slightly elevated. Compensatory stage the body is attempting to increase cardiac output to restore tissue perfusion and oxygenation. The client exhibits narrowed pulse pressure, hypotension, tachycardia, restlessness, and apprehension as acidosis develops. (BODY TRYING TO FIX THE PROBLEM) Progressive stage as compensatory mechanisms to begin to fail the client experiences severe oliguria and declining level of consciousness. Tissues and organs become hypoxic. The pulse becomes weak and thready. (BODY FAILING AT FIXING THE PROBLEM)
- Deliver warmed crystalloid fluid resuscitation (Ringer’s lactate or normal saline).
- Administer blood products (packed cells, fresh frozen plasma, and platelets). Important! The ratio of infusion should be 3:1. For every 1 ml blood loss, 3 ml of crystalloid fluid should be given. Once blood loss reaches 1500 ml, packed red cells should be administered with fresh frozen plasma and platelets to restore clotting factors. Medications
- Support blood pressure and increase cardiac contractility (inotropes). Important! Volume must be replaced first. Other Nursing Actions
- Monitor intake and output, vital signs, hemodynamic parameters, and laboratory studies.
- Increase arterial oxygenation saturation with supplemental oxygen or mechanical ventilation.
- Use supine positioning for unstable clients. DISTRIBUTIVE SHOCK: ANAPHYLACTIC
- Distributive shock results in widespread vasodilation and increased capillary permeability. Vasodilation leads to the pooling of blood in the vessels, tissue hypoperfusion, and impaired cellular metabolism. There are three types of distributive shock: neurogenic, septic, and anaphylactic.
• Rapid, weak pulse
• Skin rash
• Nausea/Vomiting
• Angioedema
• Respiratory distress
AIRWAY – EPINEPHRINE - FLUIDS
Anaphylactic Shock Anaphylactic shock is a life-threatening hypersensitivity reaction to an exogenous agent. The reaction quickly leads to massive vasodilation, the release of vasoactive mediators, and an increase in capillary permeability. Fluid leaks from the intravascular space to the interstitial space, resulting in relative hypovolemia and decreased cardiac output. Laryngeal edema and severe bronchospasm cause respiratory distress. Classic symptoms include tachycardia, dyspnea, dizziness, chest pain, swelling of lips and tongue, wheezing, and stridor. The skin appears flushed with pruritus and urticaria. Lack of oxygen leads to confusion and anxiety. If the cascade is not stopped quickly, shock results. Anaphylactic Shock The hallmark of anaphylactic shock is the sudden onset of respiratory distress. The client may have a history of allergies. Anaphylactic Shock
- Patent airway needs to be maintained. Intubation may be necessary.
- Epinephrine is the drug of choice and causes vasoconstriction and bronchodilation. It opposes the effect of histamine.
- Aggressive intravenous (IV) fluid resuscitation is needed.
- Diphenhydramine and histamine receptor blockers are used to block the ongoing release of histamines. Corticosteroids may be used as well. DISTRIBUTIVE SHOCK: NEUROGENIC
Low blood pressure Pale, cool extremities – later Difficulty breathing Decreased urine output Mental confusion O2, IV FLUIDS, ANTIBIOTICS Septic Shock Septic shock is an inflammatory response that overwhelms the immune system and results in profound circulatory, cellular, and metabolic abnormalities with an increased mortality rate. Most often, gram-positive or negative bacteria lead to sepsis, which can result in systemic inflammatory response syndrome (SIRS). As the body becomes overwhelmed, septic shock develops. Classic signs are tachypnea, tachycardia, and hypotension, despite fluid resuscitation. Blood volume is adequate but misplaced. Vasodilation occurs, capillary permeability increases, and fluid moves to the interstitial space, resulting in relative hypovolemia and decreased cardiac output. Respiratory failure is common. Hyperventilation is a compensatory mechanism, causing respiratory alkalosis. Once the client can no longer compensate, respiratory acids develop quickly, leading to respiratory failure. Temperature may be low or high. The skin will initially be warm and flushed, and then later cool and mottled. Septic Shock
- A large amount of intravenous (IV) fluid replacement is needed to restore intravascular volume and organ perfusion. Hemodynamic monitoring and strict intake/output are used to determine the adequacy of treatment.
- Vasopressors (norepinephrine) may be added if the client is no longer responsive to fluid replacement. Dobutamine is often needed to increase stroke volume and tissue perfusion.
- Vasopressin is administered to replace stores of endogenous vasopressin that are depleted in septic shock.
- Corticosteroids and antipyretics may be used.
- A proton pump inhibitor is administered to prevent stress ulcers and deep vein thrombosis (DVT) prophylaxis.
- Blood glucose levels need to be maintained below 180 mg/dL.
- Broad spectrum antibiotics are needed and should be initiated within the first hour. Blood cultures are obtained before starting antibiotics; however, the initiation of antibiotics should not be delayed beyond one hour. Question: Cardiogenic shock can result from a variety of issues. In addition to the previous myocardial infarction, identify other potential causes.
- Cardiac tamponade
- Valvular disorder
- Severe hypotension
- Dysrhythmia Nursing responsibilities in preparing for this arterial line procedure
- Zero reference the transducer
- Assess patients’ most recent serum electrolytes/coagulation profiles
- Prime and pressurize the flush tubing for the arterial catheter
- Have patient sign consent form INTRODUCTION TO ACUTE RENAL FAILURE Prerenal – decreased blood to the kidneys (BEFORE KIDNEY) Intrarenal – damage to nephron (IN THE KIDNEY) Postrenal – obstruction (AFTER THE KIDNEY) Renal failure is partial or complete impairment of kidney function. As a result, the body is unable to excrete metabolic waste products and water, causing fluid, electrolyte, and acid-base imbalance. Consequently, all body systems are affected. Renal failure is classified as acute or chronic. Acute renal failure, also called acute kidney injury (AKI), has a rapid onset, can be fatal, and requires intensive treatment to prevent chronic kidney failure. If recognized and treated early, AKI is reversible. This discussion about AKI requires an understanding of kidney anatomy and basic renal function.
intensive treatment to prevent chronic kidney failure. If recognized and treated early, AKI is reversible. This discussion about AKI requires an understanding of kidney anatomy and basic renal function. Prerenal AKI occurs before the kidney is reached. Examples include renal vein/artery stenosis and hypotension (volume depletion, decreased cardiac output). Intrarenal AKI occurs inside the kidney. Examples include overuse of non- steroidal anti-inflammatory drugs (NSAIDs), direct damage from trauma, nephrotoxins, or glomerulonephritis. Postrenal AKI occurs after the kidney. Examples include benign prostatic hyperplasia (BPH), renal stones, and spinal cord injury. Acute kidney injury (AKI) can range from slight deterioration in function to severe impairment and is characterized by a rapid loss of kidney function. Loss of function is accompanied by:
- elevated serum creatinine
- decreased urine output
- elevated blood urea nitrogen (BUN)
- elevated serum potassium Though potentially reversible, AKI has a higher mortality rate as it is typically associated with other life-threatening conditions, such as shock, embolism, heart failure, burns, hemorrhage, lupus, cancer, spinal cord injury, and nephrotoxins. When a client does not recover from AKI, chronic kidney disease may develop. Fluid Volume Hypovolemia can worsen all forms of AKI. Fluid replacement is enough to treat most forms of AKI, especially prerenal. However, as urine output decreases, fluid retention occurs, causing neck vein distention with bounding pulses. Edema and hypertension may develop, leading to heart failure and pulmonary edema Metabolic Acidosis
Impaired kidneys cannot excrete hydrogen ions. Serum bicarbonate decreases from defective reabsorption and regeneration. Serum bicarbonate is depleted through buffering of acidic hydrogen ions, and the client develops metabolic acidosis. In severe acidosis, Kussmaul respirations occur to compensate by increasing CO 2 exhalation. Sodium Balance Damaged tubules cannot conserve sodium. Urinary sodium loss increases, resulting in hyponatremia. Uncontrolled hyponatremia or fluid overload can lead to cerebral edema. Potassium Excess In AKI, serum potassium levels rise because of the kidney’s inability to excrete potassium. Tissue trauma, hemorrhage, and metabolic acidosis further increase serum potassium levels. Emergency treatment is needed for hyperkalemia to avoid cardiac dysrhythmias. Hematologic Disorders AKI may cause leukocytosis. The most common cause of death in AKI is infection, typically of the urinary or respiratory system. Neurologic Disorders As nitrogen waste products accumulate in the brain, neurologic changes may occur such as fatigue and difficulty concentrating, and progress to seizures and coma. PHASES OF ACUTE KIDNEY INJURY Oliguric – little urine Diuretic – lots of urine Recovery – GFR increases & BUN/Creatinine decrease) Clinically, AKI progresses through three phases: oliguric, diuretic, and recovery. If the client does not recover from AKI, chronic kidney disease (CKD) develops. Click on each tab to learn more about the three phases of AKI. Oliguria Oliguria, a reduction in urine output of less than 400 mL/day, occurs within the first 1 to 7 days after injury. If the cause is ischemia, oliguria onset begins
- Hemofiltration , also called continuous renal replacement therapy, (CRRT) is a form of hemodialysis used to manage unstable, critically ill clients. Instead of dialyzing up to 4 hours daily, CRRT runs continuously 24 hours per day to slowly remove waste products and fluid. Dialysis is necessary when the client’s uremia can no longer be treated with conservative medical management. Evidence of the need for dialysis includes:
- glomerular filtration rate (GFR) less than 15 mL/min
- complications, such as encephalopathy, hyperkalemia, pericarditis HOW TO ASSESS AV FISTULA Nursing Assessment of AV Fistula (Clinical Assessment) Use the Look, Listen, Feel approach. 1. LOOK (Inspection) Assess the fistula site for: Redness (infection) Swelling or edema Bleeding or drainage Bruising or hematoma Skin breakdown or ulcer Dilated veins (expected in mature fistula) Signs of infection: o Warmth o Pus o Fever Abnormal findings → report immediately. 2. LISTEN (Auscultation) Use a stethoscope over the fistula.
Normal finding: Bruit = continuous whooshing sound Abnormal findings: No bruit → possible clot or blockage (EMERGENCY) High-pitched bruit → possible stenosis Intermittent bruit → decreased blood flow
3. FEEL (Palpation) Lightly palpate using fingertips. Normal finding: Thrill = vibration or buzzing sensation Abnormal findings: No thrill → fistula may be occluded (EMERGENCY) Weak thrill → decreased blood flow Strong bounding pulse → possible stenosis 4. Assess Circulation Distal to Fistula Check: Capillary refill Skin temperature Color Pulse distal to fistula Sensation and movement Abnormal signs: Cold hand Pale hand Numbness Tingling May indicate steal syndrome
