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0133427269 Module01 Acid-Base LectureOutline

Brandeis University
Uploaded: 7 years ago
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Category: Medicine
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Filename:   0133427269_Module01_Acid-Base_LectureOutline.doc (154.5 kB)
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Module 1 AcidBase Balance The Concept of AcidBase Balance Acid-base balance ( critical to homeostasis and optimal cellular function Hydrogen determines acidity of body fluids Acids release hydrogen ions Bases accept hydrogen ions Hydrogen ion (H) concentration Measured as pH Separates to carbon dioxide (gas) and water Nonvolatile acids metabolized or excreted Lactic acid from cellular destruction Hydrochloric acid from stomach secretions Phosphoric acid from oxidation Buffer systems Prevent major changes in pH Bind with hydrogen ions when excess acid present Release hydrogen if body fluids too alkaline or basic Phosphate buffer system Inorganic Intracellular fluid (ICF) Protein buffers Extracellular fluid (ECF) ICF for organic acids produced by cellular metabolism Hemoglobin buffers H when carbonic acid dissociates Respiratory system Regulates carbonic acid by eliminating or retaining CO2 CO2 potential acid Increase in CO2 or H stimulates respiratory center, increasing respiration rate (RR) and depth of respiration Eliminates CO2 and carbonic acid to increase pH to normal range Kidneys eliminate nonvolatile acids Regulate bicarbonate (HCO3) in ECF by absorbing or regenerating HCO3 ions in tubules Slower Selective excrete or retain H ions and HCO3 ions to maintain NL pH PaCO2 measures pressure of dissolved CO2 in blood Normal value 80100 mmHg PaO2 less than 80 mmHg hypoxemia PaO2 valuable for evaluating respiratory function, acidbase balance Serum bicarbonate (HCO3)reflects regulation of acidbase balance Normal HCO3 is 22-26 mEq/L Base excess (BE) is a calculated value (buffer base capacity) Reflects degree of imbalance Indicates bodys total buffering capacity Represents amount of acid or base required to achieve pH of 7.4 Measure of increased or decreased bicarbonate Normal value for BE for arterial blood is (3.0 to 3.0 Arterial blood gases (ABGs) Assesses acidbase balance Arterial blood reflects acidbase balance throughout entire body Venous/capillary blood has dispersed O2 and collected CO2 Also provides information about effective oxygenation See CONCEPTS RELATED TO ACID-BASE BALANCE, p. 5 Alterations to acid-base balance Two major categories Acidosis H increase above normal (pH below 7.35) Alkalosis H decreases below normal (pH above 7.45) Further classification Metabolic acidosis Primary change is concentration of bicarbonate Bicarbonate decreased in relation to amount of acid in the body Result of abnormal bicarbonate losses/excess nonvolatile acids in body pH below 7.35 bicarbonate concentration 22 mEq/L Metabolic alkalosis Primary change is concentration of bicarbonate Excess of bicarbonate in relation to amount of hydrogen ion pH above 7.45 Bicarbonate concentration is greater than 26 mEq/L Respiratory acidosis Primary change is in concentration of carbonic acid CO2 lost pH rises above 7.45 PaCO2 is less than 35 mmHg Any condition that causes hyperventilation often results in respiratory alkalosis Primary (simple) Due to one cause Respiratory failure often causes respiratory acidosis due to retained CO2 Renal failure usually causes metabolic acidosis due to retained H and impaired bicarbonate production See Table 11 COMMON CAUSES OF PRIMARY ACIDBASE IMBALANCES, p. 9 Mixed disorders Combination of respiratory and metabolic disturbances Client with cardiac arrest develops mixed respiratory and metabolic acidosis Alterations and therapies See ALTERATIONS AND THERAPIES, p.8 Compensation Compensatory changes occur to restore normal pH and homeostasis Change in pH affects rate and depth of respirations This affects CO2 elimination and the PaCO2 to restore ratio of carbonic acid to bicarbonate Kidneys compensate for simple respiratory imbalances Changes in respirations occur within minutes of change in pH There are many underlying causes Each imbalance is treated separately Metabolic acidosis ( occurs in those with insulin-dependent diabetes mellitus, chronic renal failure, or severe diarrhea especially in children and older adults Metabolic alkalosis ( occurs in clients in acute care, with older adults at risk because of fragile fluid and electrolyte status Respiratory acidosis ( affects all ages with alveolar hypoventilation occurs clients with COPD at highest risk Respiratory alkalosis ( older adults and young children at greatest risk with large-dose salicylate ingestion often misidentified in older adults because early symptoms of hyperventilation and altered mental status are attributed to other disease processes Case Study A ( Jay James is a 24-year-old male who is rock climbing with friends . . . Assessment Nursing assessment Health history ( determine underlying acid-base imbalance each disorder has different symptoms important to identify prescription and OTC medications Physical assessment ( vital signs, pulse oximetry correlated with ABG results Lifespan and cultural considerations Infants, children, and older adults at risk for acid-base disorders related to fluid and electrolyte imbalances Infants and children ( at high risk due to immature kidneys that cannot concentrate urine have rapid respiratory rates that can lead to insensible losses Older adults ( at high risk because of decreased ability of kidneys to concentrate urine, decreased thirst sensation, and decreased levels of intracellular fluid also older adults have more comorbidities such as hypertension, heart disease, renal impairment, and dementia Diagnostic tests ABGs Evaluate acidbase balance and oxygenation Drawn by lab tech, respiratory therapy, or nurses with specialized skills High-pressure arterial site Apply pressure for 5 minutes (1015 if client anticoagulated) Reduce risk of bleeding or bruising Interpreting ABGs Use systematic approach Evaluate each individual measurement Analyze interrelationships to determine clients acidbase status See Box 11 INTERPRETING ABGs, p. 11 Case Study B ( Anna Zemakis is a 49-year-old female who was admitted to the hospital with severe vomiting and muscle weakness. Interventions and therapies Goal of treatment to restore or maintain normal body balance Depends on identification of underlying cause Collaborative care dependent on identification of underlying cause Health history ( needs to reflect conditions potentially related to culture and developmental stages Independent Daily weight Monitoring of intake and output Assessment of respiratory and renal function Maintenance of intact airway Oxygen saturation monitoring Vital sign measurement Assessment of level of consciousness and neurological function Prompt reporting of changes in client condition Collaborative Pharmacologic therapies ( acidosis Irritability Confusion Cyanosis Slow respirations Irregular pulse Muscle weakness Hold medication and notify healthcare provider Nurses role Monitor client condition Analyze ABG reports Assess client for symptoms associated with acidosis Assess for causative factors Contraindications and precautions High sodium content Use judiciously in clients with cardiac disease Use judiciously in clients with renal impairment Alkalinize urine Speed excretion of acidic substances Drug overdoses Chronic renal failure Kidneys not excreting H ions Sodium bicarbonate IV causes urine to become more alkaline Less acid reabsorbed in renal tubules More acid and acidic medicine excreted Called ion trapping Monitor clients acidbase status Support critical body functions that may be impaired because of drug overdose Home remedy Relieve heartburn, sour stomach related to gastric acid Client teaching Contact primary healthcare provider if gastric discomfort continues Accompanied by chest pain, dyspnea, or diaphoresis Use nonsodium antacids Do not use any antacid for longer than 2 weeks without consulting healthcare provider Pharmacologic therapies ( alkalosis Mild Administering sodium chloride concurrently with potassium chloride Combination increases renal excretion of bicarbonate ion Severe Infusions of acidic drug, i.e. ammonium chloride Nurses role Monitor clients condition Provide education to clients and their families Assess pH in ABG reports PRIOR t administration Major treatment for metabolic or respiratory alkalosis is correcting underlying disease condition Ammonium chloride only when alkalosis life threatening Contraindicated in liver disease Liver function necessary to convert ammonium ions to urea Assess for metabolic acidosis Assess for symptoms of toxic levels of ammonium chlorides Immediately discontinue infusion and contact healthcare provider Monitor renal status Monitor IV infusion site closely Acidify urine Speeds excretion of alkaline substances Ion trapping agent in treatment of drug overdose Amphetamines Phencyclidine (PCP/angel dust) Monitor acidbase status Support critical body functions compromised by drug overdose Client teaching Goals of therapy Reasons for obtaining baseline data Possible drug side effects Points to include Report pain at IV site Oral administration Parenteral administration Take ammonium chloride tablets for no longer than 6 days Report severe GI upset Fever or chills Changes in stool or urine color Take medication after meals Airway management Clients experiencing respiratory distress may require intubation Intubation generally indicated if PaCO2 is greater than 77 mmHg, PaO2 less than 60 mmHg, and pH is less than 7.20 Clients with chronic hypercarbia must be corrected slowly as correcting PaCO2 too quickly may result in metabolic alkalosis Clients who are hypoxemic may require supplemental oxygen Case Study C ( John Quinland is a 60-year-old male with a 45-year history of smoking two packs of cigarettes a day. Review The Concept of Acid-Base Balance Relate Link the Concepts Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study D ( Maria Hernandez is an 80-year-old female who was admitted to the ICU following a motor vehicle collision. Exemplar 1.1 Metabolic Acidosis Overview of metabolic acidosis Characterized by a low pH (7.35) Low bicarbonate (22 mEq/L) May be caused by excess acid in body May be caused by loss of bicarbonate from the body Respiratory system attempts to return pH to normal Increase rate Excessive losses Vomiting Suctioning Diarrhea Ileostomy drainage Fistula Hyperchloremic acidosis Excess chloride solutions infused Cause rise in chloride concentrations Renal disease Certain diuretics Normal anion gap Effects Depresses cell membrane excitability, affecting neuromuscular function Increases free calcium in ECF Clinical manifestations General manifestations Weakness Fatigue Headache General malaise GI manifestations Diminished appetite Nausea Vomiting Abdominal pain Neurologic manifestations Decline in level of consciousness Stupor Coma Cardiac manifestations Dysrhythmias Cardiac arrest Integumentary manifestations Skin often warm Flushed Skeletal manifestations Chronic acidosis Calcium released from bones Phosphate released from bones Manifestations of compensatory mechanisms Kussmaul respirations Shortness of breath Dyspnea See CLINICAL MANIFESTATIONS AND THERAPIES Metabolic Acidosis, p. 14. Collaboration Focus is on treating primary disorder Decreasing effects of acidosis on cardiac function Ensuring adequate oxygenation Diagnostic tests ABGs Serum electrolytes Tests as indicated Pharmacologic therapy Alkalinizing solution pH 7.2 Sodium bicarbonate most common Lactate, citrate, acetate solutions Metabolized to bicarbonate Given IV Oral route for chronic acidosis Monitor client Diabetic ketoacidosis IV insulin Fluid replacement Alcoholic ketoacidosis Saline solutions Glucose Lactic acidosis Correct underlying problem (shock, cardiac arrest) Improve tissue perfusion Chronic renal failure Mild to moderate metabolic acidosis Treatment dependent on pH and bicarbonate levels Diarrhea Correct underlying cause Provide fluid and electrolyte replacement Nursing process Assessment Health history Current manifestations Diminished appetite Nausea Vomiting Abdominal discomfort Fatigue Lethargy Duration of symptoms Precipitating factors Diarrhea Ingestion of toxin Chronic disease Diabetes Renal failure Cirrhosis of the liver Endocrine disorder Current medications Physical assessment Mental status and level of consciousness (LOC) Vital signs Include respiratory rate and depth Apical and peripheral pulses Skin color and temperature Abdominal contour Note distention Bowel sounds Urine output Diagnosis Focus on primary disorder Possible nursing diagnoses for effects of acidosis Decreased Cardiac Output Risk for Excess Fluid Volume Risk for Injury Planning Identification and treatment of underlying cause Restoration and maintenance of acidbase balance Nursing care includes measure to treat underlying disorders Refer to other concepts Potential goals for clients with metabolic acidosis Client will describe and demonstrate preventive measures related to chronic disease process pH will remain within normal range Disease process causing acidbase imbalance will be controlled to reduce acid production or alkaline loss Client will maintain vital signs within normal range for age and condition Client will maintain baseline cardiac rhythm Client will maintain or regain normal serum electrolyte levels Implementation Monitor cardiac status Monitor vital signs, including peripheral pulses and capillary refill Hypotension Diminished pulse strength Slowed capillary refill Increases risk for lactic acidosis Monitor ECG pattern for dysrhythmias and hypokalemic changes Monitor and maintain fluid replacement as ordered Monitor serum sodium levels and osmolality Bicarbonate administration can cause hypernatremia and hyperosmolality Leads to water retention Monitor heart sounds Third heart sound (S3) due to volume of blood flow through the heart Monitor central venous pressure (CVP) High CVP readings indicative of hypervolemia Report to care provider Monitor respiratory status Increasing dyspnea Adventitious lung sounds Report to care provider Assess for edema Dependent tissues Periorbital indicates generalized edema Assess urine output hourly Maintain accurate intake and output records Note urine output 30 mL/hr Note positive fluid balance on 24-hour total intake and output calculations Heart failure and inadequate renal perfusion may lead to decreased urine output Obtain daily weights using consistent conditions Same scale Indicator of fluid balance Administer prescribed diuretics Monitor response to therapy Loop/high-ceiling diuretics can lead to further electrolyte imbalance Reduce risk for injury Monitor neurological function Mental status LOC Muscle strength As pH falls, mental function declines Institute safety precautions Keep bed at lowest position possible Side rails raised Orient to time place and circumstances as needed Keep clocks, calendars, and familiar objects at bedside Allow significant others to remain with client as much as possible Client maintains pH within normal range Monitor pH frequently Clients vital signs remain within normal range based on age and condition Monitor frequently Client maintains adequate oxygenation of tissues Client is able to describe or demonstrate measures to control disease process to prevent future complications of pH imbalance Review Metabolic Acidosis Relate Link the Concepts and Exemplars Ready Go to the Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 1.2 Metabolic Alkalosis Overview Characterized by high pH (7.45) And a high bicarbonate (28 mEq/L) May be caused by loss of acid or excess bicarbonate in body Respiratory system attempts to return pH to normal by slowing respiratory rate CO2 retained PaO2 increases (45 mmHg) Pathophysiology and etiology High bicarbonate Hydrogen ions lost Via gastric secretions Vomiting or gastric suctioning Gastric secretions highly acidic (pH 13) When H lost, alkalinity of body fluids increases High pH depresses the respiratory system as body retains CO2 Risk factors Rarely occurs as primary disorder Hospitalization Hypokalemia Treatment with bicarbonate Clinical manifestations Result of calcium ionization Similar to hypocalcemia Numbness and tingling around mouth, fingers toes Dizziness Trousseau sign Muscle spasm Aimed at controlling alkalosis Treating underlying cause Pharmacologic therapy Restoring normal fluid volume Administer potassium chloride solution Restores serum and intracellular potassium levels Allows kidneys to conserve hydrogen ions more effectively Administer sodium chloride solution Promotes renal excretion of bicarbonate Restore fluid volume deficits that can contribute to metabolic alkalosis Severe alkalosis Acidifying hydrochloric acid or ammonium chloride may be administered Kidneys selectively retain potassium and excrete H to restore ECF potassium levels Urinary chloride levels may be normal or greater than 250 mEq/24 hours ECG pattern shows changes similar to those seen with hypokalemia See Exemplar 6.3 Fluid and Electrolyte Imbalance for more information related to symptoms of hypokalemia Changes may be due to hypokalemia or the alkalosis Nursing Process Assessment Health history Current manifestations Numbness and tingling Muscle spasms Dizziness Duration of symptoms Precipitating factors Ingestion of bicarbonate Vomiting Diuretic therapy Endocrine disorders Current medications Physical assessment Vital signs Diagnostic tests ABGs Serum electrolytes Diagnosis Risk for Impaired Gas Exchange Respiratory compensation depresses the respiratory rate Reduces the depth of breathing to promote CO2 retention Deficient Fluid Volume Risk for Injury Planning Depends on identification and treatment of underlying cause Restoring and maintaining normal acidbase balance Nursing care Includes measures to treat underlying disorder Appropriate outcomes Return to oxygen saturation level of 93 or greater Return to normal or near normal fluid and electrolyte volumes 4, Implementation Monitor for impaired gas exchange Monitor respiratory rate and effort Note and report cyanosis around the mouth (circumoral cyanosis) Indicates significant hypoxia Monitor mental status and LOC Report decreasing LOC Report behavior changes May be early signs of hypoxia Place in semi-Fowler or Fowler position as tolerated Facilitates alveolar ventilation Facilitates gas exchange Administer O2 as ordered Maintain O2 saturation levels Maintain blood and tissue oxygenation in spite of depressed respirations Schedule nursing care activities to allow rest periods Limited energy reserves in hypoxemic client Frequent rest with limited activities Monitor for fluid volume deficit Assess intake and output accurately Monitor fluid balance Hourly intake and output in acute situations Urine output of less than 30 mL/hr indicates inadequate tissue perfusion Inadequate renal perfusion Increased risk for acute renal failure Assess vital signs, CVP, and peripheral pulse volume at least every 4 hours for signs of hypovolemia Hypotension Tachycardia Low CVP Weak, easily obliterated peripheral pulses Weigh daily under standard conditions Rapid weight changes accurately reflect fluid balance Administer IV fluids as prescribed Use electronic infusion pump If rapid fluid replacement ordered, monitor for signs of fluid overload Dyspnea Tachypnea Tachycardia Increased CVP Jugular vein distention Edema Hypervolemia may result in pulmonary edema, cardiac failure Monitor serum electrolytes, osmolality, and ABG values Rehydration and administration of potassium chloride Affect both acidbase balance Affect fluid and electrolyte balance Care in the community Consider the cause of alkalosis and underlying factors Teaching about the following Using appropriate antacids for heartburn and gastric distress Using potassium supplements as ordered Eat high-potassium foods if Taking a potassium-wasting diuretic Aldosterone production impaired Contact primary care provider if uncontrolled or extended vomiting develops Evaluation Normal outcomes of nursing care relate to restoration of normal body balance Revisions of care plan may need to be made if client does not respond to some aspect of the plan Nurses may need to follow up with client re self-monitoring and self-care Possible outcomes include the following Client relates antacids that are acceptable for use and will reduce reoccurrence of metabolic alkalosis Client describes proper self-administration procedure for oral potassium supplements Client describes when to notify provider related to changes in daily weight Clients arterial pH returns to normal range Clients serum electrolyte values are within normal range Review Metabolic Alkalosis Relate Link the Concepts and Exemplars Ready Go to the Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 1.3 Respiratory Acidosis Overview of respiratory acidosis Characterized by a pH less than 7.35 PaO2 greater than 45 mmHg May be acute or chronic In chronic respiratory acidosis, bicarbonate is higher than 26 mEq/L Kidneys compensating by retaining bicarbonate Pathophysiology and etiology Result from carbon dioxide retention Both acute and chronic Alveolar hypoventilation Hypoxemia common with respiratory acidosis Acute respiratory acidosis Sudden failure of ventilation (exchange if oxygen and carbon dioxide) Chest trauma Aspiration of foreign body Acute pneumonia Overdoses of narcotic or sedative medication PaCO2 rises rapidly pH falls markedly pH of 7 or lower can occur within minutes Resulting in death if not corrected Initially serum bicarbonate level unchanged due to compensatory response of kidneys Hypercapnia (increased carbon dioxide levels) Affects neurological function CO2 crosses bloodbrain barrier rapidly Cerebral blood vessels dilate Intracranial pressure increases Papilledema (swelling and inflammation of optic nerve where it enters the retina) develops Peripheral vasodilation also occurs Pulse rate increases to maintain cardiac output Chronic respiratory acidosis Associated with chronic respiratory or neuromuscular conditions COPD Asthma Cystic fibrosis Multiple sclerosis Affects alveolar ventilation Airway obstruction Structural changes in the lung Limited chest wall expansion Majority of clients with chronic respiratory acidosis COPD with chronic bronchitis and emphysema PaO2 increases over time and remains elevated Kidneys retain bicarbonate pH often close to normal Adequate metabolic compensation Hypercapnia CO2 levels rise gradually Compensatory changes occur Respiratory center becomes less sensitive to CO2 as a stimulant of respiratory drive PaO2 provides primary stimulus for respirations At risk for carbon dioxide narcosis If respiratory center suppressed by administering excess supplemental oxygen Manifestations include Confusion Tremors Convulsions Coma if CO2 levels reach 70 mmHg or higher Carefully monitor neurological and respiratory status in clients with chronic respiratory acidosis who are receiving oxygen therapy ( immediately report a decreasing LOC or depressed respirations. Risk factors Acute lung disease Chronic lung disease Trauma Narcotic analgesics Airway obstruction Neuromuscular disease Clinical manifestations Acute respiratory acidosis PaCO2 levels rise rapidly Cause manifestations of hypercapnia Cerebral vasodilation LOC progressively decreases Rapid changes in ABGs Unconsciousness Ventricular fibrillation Skin warm, flushed Pulse elevated Treated in emergency department or ICU Chronic respiratory acidosis Weakness Dull headache Sleep disturbances ( daytime sleepiness Impaired memory Personality changes O2 administration to client with chronic hypercapnia COPDremoves respiratory drive See exemplar on COPD in Module 15 Oxygenation See CLINICAL MANIFESTATIONS AND THERAPIES Respiratory Acidosis, p. 22. Collaboration Healthcare team may include Respiratory therapist May provide breathing treatments Related therapies as ordered Pharmacistprevent contraindicated medication administration Primary care providerprevent contraindicated medication administration Dietitian Clients using accessory muscles Increased caloric needs Diagnostic tests ABGs pH 7.35 PaCO2 45 mmHg Acute respiratory acidosis Bicarbonate initially in normal range Increases to 26 mEq/L if condition persists Chronic respiratory acidosis PaCO2 may be significantly elevated HCO3 may be significantly elevated Serum electrolytes May show hypochloremia (Cl 98 mEq/L) Pulmonary function tests Determine if chronic lung disease is cause of respiratory acidosis Not during acute period Pharmacologic therapy Bronchodilator drugs O2 administered cautiously to avoid CO2 narcosis Pulmonary hygiene Deep breathing Coughing exercises Breathing treatments Percussion and drainage Adequate hydration to promote removal of respiratory secretions Nursing process Assessment Health history Current manifestations Headache Irritability Lethargy Difficulty thinking Blurred vision Duration of symptoms Precipitating factors Drug use Respiratory infection Chronic disease Cystic fibrosis COPD Current medications Physical examination Vital signs Skin color and temperature Rate and depth of respirations Pulmonary excursion Lung sounds Diagnosis Restoring effective alveolar ventilation and gas exchange is priority Possible nursing diagnoses Impaired Gas Exchange Ineffective Airway Clearance Anxiety Risk for Injury Planning Expected outcomes Resolution of underlying illness Client maintains adequate fluid intake Maintains oxygenation saturation greater than 90 Maintains normal PaCO2 level Maintains pH balance Implementation Frequently assess respiratory status Rate Depth Effort Oxygen saturation levels Decreasing respiratory rate and effort, decreasing O2 saturation may signal worsening respiratory failure and respiratory acidosis Promote gas exchange Promptly evaluate and report ABG results to physician and respiratory therapist Rapid changes in CO2 or O2 may necessitate change in treatment plan Prevent overcorrection of respiratory acidosis Place in semi-Fowler position as tolerated Administer O2 as ordered Promote effective airway clearance Frequently auscultate breath sounds Increasing or decreasing sounds may indicate worsening airway clearance Encourage client with chronic respiratory acidosis to use pursed-lipped breathing Ambulation Encourage fluid intake up to 3000 mL per day as tolerated or allowed Administer medications as ordered Pulmonary hygiene measures Reduce anxiety levels Result of hypoxia and hypercapnia Insufficient oxygen supply to neurons Anxiety often eliminated by improved ventilation and oxygenation Remain with client and monitor for changes in condition Explain procedures and treatments Reduce environmental stimuli Use calm, reassuring manner Allow supportive family members to remain with the client as much as possible Reduce risk for injury May experience blurred vision Altered LOC Assess LOC, orientation, and strength frequently Place call bells within reach Encourage client to remain in bed Administer supplemental O2 as needed Care in the community Teach client and family about preventive measures and equipment May be prevention only if acute respiratory acidosis Narcotic overdose Chronic lung diseases clients and families Provide instructions when respiratory status is compromised Evaluation Nursing care based on meeting goals Expected outcomes include Client maintains patent airway Client maintains appropriate breathing patterns to meet O2 demands Client remains conscious Client does not display anxiety indicating potential hypoxia ABGs reflect pH and PaCO2 within acceptable range for client Review Respiratory Acidosis Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 1.4 Respiratory Alkalosis Overview of respiratory alkalosis Characterized by a pH greater than 7.45 PaCO2 less than 35 mmHg Other physiological causes that may directly stimulate the respiratory center High fever Hypoxia Gram-negative bacteremia Thyrotoxicosis Early salicylate intoxication Encephalitis High progesterone level in pregnancy Mechanical ventilation and anesthesia Rate and tidal volume (depth) of respirations excessive Chronic respiratory alkalosis Neuromuscular excitability increases Manifestations similar to hypocalcemia develop Low carbon dioxide levels in the blood cause vasoconstriction of cerebral vessels Increases neurologic manifestations of the disorder Risk factors Anxiety disorders with hyperventilation Mechanical ventilation settings Breaths per minute Peak pressures Too high for clients needs Clinical manifestations Light-headedness Feeling of panic and difficulty concentrating Circumoral and distal extremity paresthesias Tremors Positive Chvostek sign (facial spasm, usually indicative of hypocalcemia) Trousseau sign (spasm of the hand and forearm) Tinnitus Sensation of chest tightness Palpitations Seizures and loss of consciousness may occur ABGs Show pH 7.45 PaCO2 less than 35 mmHg Reduce anxiety or panic ABGs before meds or O2 therapy Pharmacologic therapy Antianxiety agent Relieve anxiety Restore normal breathing pattern Respiratory therapy Paper bags can cause hypoxia Historically recommended Will help raise CO2 levels Other diseases can mimic hyperventilation Adjust ventilator settings Reduce respiratory rate Reduce peak expiratory pressure Reduce tidal volume Administer oxygen as ordered Nursing process Assessment Health history History of anxiety disorders Triggering event for onset of hyperventilation Assess for mental health disorders, coping mechanisms, support systems Physical examination Assess breath sounds Neurological function Respiratory status Cardiac status Changes in LOC Diagnosis Ineffective Breathing Pattern Anxiety Planning Identify and treat underlying cause Restore acidbase balance Appropriate outcomes include Manifest normal respiratory rate and rhythm Maintain safety Maintain appropriate fluid status Implementation Assess respiratory rate, depth, and ease Monitor vital signs and skin color Obtain subjective assessment data leading to current situation Current health and recent illnesses, medication use Current manifestations Reassure client that he or she is not experiencing a heart attack Dyspnea, chest tightness, palpitations may mimic heart attack Instruct client to maintain eye contact and breathe with nurse to slow respiratory rate Be aware that eye contact may make some clients uncomfortable Protect client from injury Refer for counseling if repeated episodes or chronic anxiety disorder Home care Underlying cause of hyperventilation Discuss anxiety and stress management Teach client how to identify a hyperventilation reaction Provide self-care Evaluation Expected outcomes include the following Client experiences no subsequent episodes of hyperventilation Client describes strategies for coping with anxiety in the future Family displays ability to contribute to calming client during times of anxiety Client and/or family participates in support groups that will help the client cope with anxiety disorder Review Respiratory Alkalosis Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study 2015 by Education, Inc. Lecture Outline for Nursing A Concept-Based Approach to Learning, 2e, Volume 1 PAGE PAGE 8 Y, dXiJ(x( I_TS 1EZBmU/xYy5g/GMGeD3Vqq8K)fw9 xrxwrTZaGy8IjbRcXI u3KGnD1NIBs RuKV.ELM2fi V vlu8zH (W uV4(Tn 7_m-UBww_8(/0hFL)7iAs),Qg20ppf DU4p MDBJlC5 2FhsFYn3E6945Z5k8Fmw-dznZ xJZp/P,)KQk5qpN8KGbe Sd17 paSR 6Q

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