Adult Health Test 2 Flashcards
Fluid and electrolyte balance
A.22-26 Bicarbonate
B.Drawn by respiratory therapists from artery. Used to treat and diagnose acid base disturbances
C.Homeostasis, necessary for life.
Homeostasis, necessary for life.
Ph range comparable with life.
A.6.8-7.8
B. >94%
C.22-26
6.8-7.8
Normal ph
A.6.8-7.8
B. 7.35-7.45
C. 35-45
7.35-7.45
Normal PaCO2 oxygen saturation of hemoglobin
A. 35-45 carbon dioxide
B. 22-26
C. 7.35-7.45
35-45 carbon dioxide
Normal HCO3
A. 6.8-7.8
B. >94%
C. 22-26 Bicarbonate
22-26 Bicarbonate
SPo2
A. >94%
B. <94%
C. >85%
> 94%
Abgs
A. Major extra cellular fluid buffer system- carbonic acid
B. Drawn by respiratory therapists from artery. Used to treat and diagnose acid base disturbances
C. Bicarbonate in ECF, can regenerate and absorb
Drawn by respiratory therapists from artery. Used to treat and diagnose acid base disturbances
Bicarbonate
A. Major extra cellular fluid buffer system- carbonic acid
B. Slow, hours or days. Take care of CO2 first since it’s faster.
C. Drawn by respiratory therapists from artery. Used to treat and diagnose acid base disturbances
Major extra cellular fluid buffer system- carbonic acid
Medulla controls?
A. Bicarbonate in ECF, can regenerate and absorb
B. Lungs
C. Kidneys
Lungs
Lungs regulate?
A. K+
B. PH
C. Co2
Co2
Kidneys regulate
A. PH
B. Bicarbonate in ECF, can regenerate and absorb
C. NA+
Bicarbonate in ECF, can regenerate and absorb
How fast is renal compensation?
A. Slow, hours or days. Take care of CO2 first since it’s faster.
B. Fast
C. Increases, increasing elimination of CO2 (reducing acid load)
Slow, hours or days. Take care of CO2 first since it’s faster.
In metabolic acidosis what does the respiratory rate do?
A. AG=NA+ + K+ -(CL- + HCO3-) or AG=Na+ - (Cl- + HCO3-)
Second used more often than the first.
B. Bicarbonate-carbonic acid
C. Increases, increasing elimination of CO2 (reducing acid load)
Increases, increasing elimination of CO2 (reducing acid load)
In metabolic alkalosis what does the respiratory rate do?
A. Decreases causing retention of CO2, increasing acid loss.
B. Increases, increasing elimination of CO2 (reducing acid load)
C. Value calculated from multiple medical lab tests. (8-12mEq/L w/o K+, 12-16 mEq/L with K+
Decreases causing retention of CO2, increasing acid loss.
What is the most common buffer system in the body?
A. pH
B. Bicarbonate
C. B/P
Bicarbonate
What is the serum anion gap?
A. AG=NA+ + K+ -(CL- + HCO3-) or AG=Na+ - (Cl- + HCO3-)
Second used more often than the first.
B. pH <7.35, HCo3 <22 mEq//L (due to kidney injury) or N/V
C. Value calculated from multiple medical lab tests. (8-12mEq/L w/o K+, 12-16 mEq/L with K+
Value calculated from multiple medical lab tests. (8-12mEq/L w/o K+, 12-16 mEq/L with K+
What is the anion gap calculation?
A. AG=NA+ + K+ -(CL- + HCO3-) or AG=Na+ - (Cl- + HCO3-)
Second used more often than the first.
B. Value calculated from multiple medical lab tests. (8-12mEq/L w/o K+, 12-16 mEq/L with K+
C. HA, confusion, drowsiness, (Inc resp. rate and depth) Dec. B/P, Dec. cardiac output, dysrhythmias, shock
AG=NA+ + K+ -(CL- + HCO3-) or AG=Na+ - (Cl- + HCO3-)
Second used more often than the first.
Lab values of Metabolic Acidosis
A. AG=NA+ + K+ -(CL- + HCO3-) or AG=Na+ - (Cl- + HCO3-)
B. pH <7.35, HCo3 <22 mEq//L (due to kidney injury) or N/V
C. HA, confusion, drowsiness, (Inc resp. rate and depth) Dec. B/P, Dec. cardiac output, dysrhythmias, shock.
pH <7.35, HCo3 <22 mEq//L (due to kidney injury) or N/V
Symptoms of Metabolic Acidosis
A. Watch for hyperkalemia (monitor potassium) and look for hypocalcemia, Cardiac monitor, if due to chronic renal failure may need treatment with hemodialysis, or peritoneal dialysis.
B. HA, confusion, drowsiness, (Inc resp. rate and depth) Dec. B/P, Dec. cardiac output, dysrhythmias, shock.
C. >7.45 PH, >26 Bicarb (Vomiting, and gastric suction, or long-term diuretic use)
HA, confusion, drowsiness, (Inc resp. rate and depth) Dec. B/P, Dec. cardiac output, dysrhythmias, shock.
Treating Metabolic Acidosis
A. Watch for hyperkalemia (monitor potassium) and look for hypocalcemia, Cardiac monitor, if due to chronic renal failure may need treatment with hemodialysis, or peritoneal dialysis.
B. Hypokalemia (prominent U waves), symptoms of dec. calcium, resp. depression, Tachycardia, and symptoms of hypokalemia. Test urine chloride levels, leads up to paralytic ileus, or decreased motility.
C. Administer Bicarb.
Administer Bicarb.
Nursing Treatment, Metabolic acidosis
A. Watch for hyperkalemia (monitor potassium) and look for hypocalcemia, Cardiac monitor, if due to chronic renal failure may need treatment with hemodialysis, or peritoneal dialysis.
B. Administer Bicarb.
C. Before treating Met. Acid. , to avoid tetany
Watch for hyperkalemia (monitor potassium) and look for hypocalcemia, Cardiac monitor, if due to chronic renal failure may need treatment with hemodialysis, or peritoneal dialysis.
Correct Electrolytes in Metabolic Acidosis
A. Before treating Met. Acid. , to avoid tetany
B. Hypokalemia (prominent U waves), symptoms of dec. calcium, resp. depression, Tachycardia, and symptoms of hypokalemia. Test urine chloride levels, leads up to paralytic ileus, or decreased motility.
c. Watch for hyperkalemia (monitor potassium) and look for hypocalcemia, Cardiac monitor, if due to chronic renal failure may need treatment with hemodialysis, or peritoneal dialysis.
Before treating Met. Acid. , to avoid tetany
Lab values for Metabolic Alkalosis
A. PH<7.35, Pao2 > 42 mmHg Due to inadequate excretion of co2, (hypercapnia)
B. >7.45 PH, >26 Bicarb (Vomiting, and gastric suction, or long-term diuretic use)
C. Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
> 7.45 PH, >26 Bicarb (Vomiting, and gastric suction, or long-term diuretic use)
What to look for in Metabolic Alkalosis
A. Give chloride allowing excretion of bicarb, or sodium chloride, Monitor I&O, Possibly KCL
B. PH<7.35, Pao2 > 42 mmHg Due to inadequate excretion of co2, (hypercapnia)
C. Hypokalemia (prominent U waves), symptoms of dec. calcium, resp. depression, Tachycardia, and symptoms of hypokalemia. Test urine chloride levels, leads up to paralytic ileus, or decreased motility.
Hypokalemia (prominent U waves), symptoms of dec. calcium, resp. depression, Tachycardia, and symptoms of hypokalemia. Test urine chloride levels, leads up to paralytic ileus, or decreased motility.
Treatment for metabolic alkalosis
A. Give chloride allowing excretion of bicarb, or sodium chloride, Monitor I&O, Possibly KCL
B. Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
C. Respiratory failure, sedation, sleep apnea, PE, Asthma
Give chloride allowing excretion of bicarb, or sodium chloride, Monitor I&O, Possibly KCL.
Lab values for Respiratory Acidosis
A. Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
B. PH<7.35, Pao2 > 42 mmHg Due to inadequate excretion of co2, (hypercapnia)
C. >7.45 PH, >26 Bicarb (Vomiting, and gastric suction, or long-term diuretic use)
PH<7.35, Pao2 > 42 mmHg Due to inadequate excretion of co2, (hypercapnia)
Symptoms of Respiratory Acidosis
A. Respiratory failure, sedation, sleep apnea, PE, Asthma
B. Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
C. Airway patency, Vitals, Nero. stat., cardiopulmonary stat. , Pulse ox, ABGs, serum electrolytes
Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
Causes of Respiratory acidosis
A. Respiratory failure, sedation, sleep apnea, PE, Asthma
B. Inc. pulse, inc. respiratory rate, and inc. B/P, Feeling of fullness in the head
C. Airway patency, Vitals, Nero. stat., cardiopulmonary stat. , Pulse ox, ABGs, serum electrolytes
Respiratory failure, sedation, sleep apnea, PE, Asthma
Treatment for Respiratory Acidosis
A. Airway patency, Vitals, Nero. stat., cardiopulmonary stat. , Pulse ox, ABGs, serum electrolytes
B. PH>7.45, PaCO2 <35 mm Hg (due to hyperventilation)
C. Can increase intracranial pressure, Give prescribed drugs, Bronchodilators, IV fluids as ordered, supplimental o2, Elevate HOB, Take slow deep breaths, s Relaxation and stress management, ensure airway, suction as necessary, Assist with ET tube,
Can increase intracranial pressure, Give prescribed drugs, Bronchodilators, IV fluids as ordered, supplimental o2, Elevate HOB, Take slow deep breaths, s Relaxation and stress management, ensure airway, suction as necessary, Assist with ET tube,
Monitor for Respiratory acidosis
A . Lower PH
B. Airway patency, Vitals, Nero. stat., cardiopulmonary stat. , Pulse ox, ABGs, serum electrolytes
C. Light headed, inability to concentrate, numbness and tingling, maybe LOC
Airway patency, Vitals, Nero. stat., cardiopulmonary stat. , Pulse ox, ABGs, serum electrolytes
Lab values for Respiratory Alkalosis
A. PH>7.45, PaCO2 <35 mm Hg (due to hyperventilation)
B. Slow down ventilation, Brown Bag
C. 20:1 Bicarb, to hco2
PH>7.45, PaCO2 <35 mm Hg (due to hyperventilation)
Symptoms of Respiratory Alkalosis
A. Higher PH
B. 20:1 Bicarb, to hco2
C. Light headed, inability to concentrate, numbness and tingling, maybe LOC
Light headed, inability to concentrate, numbness and tingling, maybe LOC
Treatment for Respiratory Alkalosis
A. Slow down ventilation, Brown Bag
B. Higher PH
C. 20:1 Bicarb, to hco2
Slow down ventilation, Brown Bag
Lower the H+=
A. Lower PH
B. Higher PH
C. conserve hydrogen ions, and excrete bicarb ions
Higher PH
Higher the H+=
A. Lower PH
B. Higher PH
C. Slow down ventilation, Brown Bag
Lower PH
ABGs are
A. CO2 on ECF
B. 20:1 Bicarb, to hco2
C. conserve hydrogen ions, and excrete bicarb ions
20:1 Bicarb, to hco2
Effects on Kidneys on MAcid, RAcid
A. Kidneys excrete hydrogen ions, and conserve bicarb ions
B. Resp rate inc. causing co2 to be eliminated
C. conserve hydrogen ions, and excrete bicarb ions
Kidneys excrete hydrogen ions, and conserve bicarb ions
Effects on Kidneys on Malk, Ralk
A. CO2 on ECF
B. Resp Dec. causing co2 to be retained
C. conserve hydrogen ions, and excrete bicarb ions
conserve hydrogen ions, and excrete bicarb ions
medulla controls lungs and lungs control?
A. CO2 on ECF
B. Resp Dec. causing co2 to be retained
C. two or more, Normal PH in the presence of changes in the PaCO2 and HCO3. Acidosis and Alkalosis can’t occur together.
CO2 on ECF
In metabolic acidosis
A. Resp Dec. causing co2 to be retained
B. conserve hydrogen ions, and excrete bicarb ions
C. Resp rate inc. causing co2 to be eliminated
Resp rate inc. causing co2 to be eliminated
In met. Alk.
A. Resp Dec. causing co2 to be retained
B. Collapse of aveoli
C. Resp rate inc. causing co2 to be eliminated
Resp Dec. causing co2 to be retained
Mixed Acid base disorders
A. Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
B. two or more, Normal PH in the presence of changes in the PaCO2 and HCO3. Acidosis and Alkalosis can’t occur together.
C. Insideous increasing dyspnea, cough, and sputum production.
two or more, Normal PH in the presence of changes in the PaCO2 and HCO3. Acidosis and Alkalosis can’t occur together.
Atelectasis
A. Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
B. Insideous increasing dyspnea, cough, and sputum production.
C. Collapse of aveoli
Collapse of aveoli
Symptoms of Atelectasis
A. Insideous increasing dyspnea, cough, and sputum production.
B. same as acute, due to pulmonary infection
C. Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
Insideous increasing dyspnea, cough, and sputum production.
Symptoms of acute Atelectasis
A. same as acute, due to pulmonary infection
B. Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
C. Increased work for breathing and hypoxemia, dec breath sounds and crackles over affected area, chest x-ray, pulse ox less than 90%
Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
Symptoms of Chronic Atelectasis
A. Tachycardia, tachypnea, pleural pain, and central cynosis when large portions of lungs are affected.
B. same as acute, due to pulmonary infection
C. Frequent turning, early mobilization, incentive spirometer, voluntary deep breathing, pressurized meter- dosed inhaler.
same as acute, due to pulmonary infection
Assessing and diagnosing Atelectasis
A. PEEP, CPAB, ICOUGH, CPT (hooked to vent) Intubation, Thoracentesis
B. Frequent turning, early mobilization, incentive spirometer, voluntary deep breathing, pressurized meter- dosed inhaler.
C. Increased work for breathing and hypoxemia, dec breath sounds and crackles over affected area, chest x-ray, pulse ox less than 90%
Increased work for breathing and hypoxemia, dec breath sounds and crackles over affected area, chest x-ray, pulse ox less than 90%
Nursing interventions for Atelectasis
A. Demyelination disease of the CNS ( destruction of the fatty protein material that surround certain nerve fibers in the brain and spinal cord)
B. Sudden acute life-threatening deterioration of gas exchangeto lungs. no adequate o2 or ventilation to blood (pao2<55 /, PACO2 >55, and PH <7.35
C. Frequent turning, early mobilization, incentive spirometer, voluntary deep breathing, pressurized meter- dosed inhaler.
Frequent turning, early mobilization, incentive spirometer, voluntary deep breathing, pressurized meter- dosed inhaler.
Management for atelectasis
A. PEEP, CPAB, ICOUGH, CPT (hooked to vent) Intubation, Thoracentesis
B. Trauma-Boating accidents, car accidents, pneumonia, ARDS, HF, COPD, PE, cystic fibrosis (anesthetic, analgesic, and sedative agents) or pain
C. Deteriorization in the gas exchange function of the lung that has been insideously or persisted for long periods of time after ARF (No acute SX)
PEEP, CPAB, ICOUGH, CPT (hooked to vent) Intubation, Thoracentesis
Acute Respiratory Failure
A. COPD, MS, Muscular dystrophy, Myasthenia Gravis, Gukllian barre syndrome
B. Trauma-Boating accidents, car accidents, pneumonia, ARDS, HF, COPD, PE, cystic fibrosis (anesthetic, analgesic, and sedative agents) or pain
C. Sudden acute life-threatening deterioration of gas exchangeto lungs. no adequate o2 or ventilation to blood (pao2<55 /, PACO2 >55, and PH <7.35
Sudden acute life-threatening deterioration of gas exchangeto lungs. no adequate o2 or ventilation to blood (pao2<55 /, PACO2 >55, and PH <7.35
Causes of ARF
. A, Trauma-Boating accidents, car accidents, pneumonia, ARDS, HF, COPD, PE, cystic fibrosis (anesthetic, analgesic, and sedative agents) or pain
B. COPD, MS, Muscular dystrophy, Myasthenia Gravis, Gukllian barre syndrome
C. Deteriorization in the gas exchange function of the lung that has been insideously or persisted for long periods of time after ARF (No acute SX)
Trauma-Boating accidents, car accidents, pneumonia, ARDS, HF, COPD, PE, cystic fibrosis (anesthetic, analgesic, and sedative agents) or pain
Chronic Respiratory failure
A. Bilateral infiltration, sever dyspnea, Racing heart, Retractions, hypoxia, tachycardia, Crackles (ABG dyspnea
B. Deteriorization in the gas exchange function of the lung that has been insideously or persisted for long periods of time after ARF (No acute SX)
C. Life threatening and resembles severe pulmonary edema, Inflammatroy process causing damage to aveoli, leading to sudden and progressive pulmonary edema
Deteriorization in the gas exchange function of the lung that has been insideously or persisted for long periods of time after ARF (No acute SX)
Causes of Chronic Respiratory failure
A. Retractions, hypoxia, tachycardia, Crackles (ABG dyspnea
B. Massive trauma, Severe respiratory disorder, Prolonged mechanical ventilation, Hemorrhage shock, Fat embolism (due to broken bone), Septic condition
C. COPD, MS, Muscular dystrophy, Myasthenia Gravis, Gukllian barre syndrome
COPD, MS, Muscular dystrophy, Myasthenia Gravis, Gukllian barre syndrome
Acute Respiratory distress syndrome
A. Life threatening and resembles severe pulmonary edema, Inflammatroy process causing damage to aveoli, leading to sudden and progressive pulmonary edema S
B. PEEP,
C. Rapid onset of severe dyspnea, within 72 hours of incident.Rapid onset of severe dyspnea, within 72 hours of incident.
Life threatening and resembles severe pulmonary edema, Inflammatroy process causing damage to aveoli, leading to sudden and progressive pulmonary edema S
Characterizations of ARDS
A. Massive trauma, Severe respiratory disorder, Prolonged mechanical ventilation, Hemorrhage shock, Fat embolism (due to broken bone), Septic condition
B. Bilateral infiltration, sever dyspnea, Racing heart, Retractions, hypoxia, tachycardia, Crackles (ABG dyspnea
C, REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
Bilateral infiltration, sever dyspnea, Racing heart, Retractions, hypoxia, tachycardia, Crackles (ABG dyspnea
Treating ARDS
A. REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
B. Rapid onset of severe dyspnea, within 72 hours of incident.
C. PEEP,
PEEP,
Acute phase of ARDS
A. Rapid onset of severe dyspnea, within 72 hours of incident.
B. Prepare to intubate, Monitor co2, Secretions, ABG’s, Turning, mouth care, ROM, Prone positioning, enteral feedings,
C. REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
Rapid onset of severe dyspnea, within 72 hours of incident.
Cause of ARDS
A, Common (Pneumonia, Aspiration of gastric contents) Uncommon (Pulmonary contusion, Near drowning, Inhalation injury, fat embolism, reperfusion injury)
B. Massive trauma, Severe respiratory disorder, Prolonged mechanical ventilation, Hemorrhage shock, Fat embolism (due to broken bone), Septic condition
C. REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
Massive trauma, Severe respiratory disorder, Prolonged mechanical ventilation, Hemorrhage shock, Fat embolism (due to broken bone), Septic condition
Symptoms of ARDS
A. Common (Pneumonia, Aspiration of gastric contents) Uncommon (Pulmonary contusion, Near drowning, Inhalation injury, fat embolism, reperfusion injury)
B. Prepare to intubate, Monitor co2, Secretions, ABG’s, Turning, mouth care, ROM, Prone positioning, enteral feedings,
C. REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
REstless, HA, dyspnea, Air hunger, tachycardia, inc. B/P
Treatment for ARDS
A. Common (Sepsis, Severe trauma with shock, Multiple transfusion) Uncommon (Post cardiac surgery, Pancreatitis, drug overdose, After massive rransfusion)
B. Prepare to intubate, Monitor co2, Secretions, ABG’s, Turning, mouth care, ROM, Prone positioning, enteral feedings,
C. Common (Pneumonia, Aspiration of gastric contents) Uncommon (Pulmonary contusion, Near drowning, Inhalation injury, fat embolism, reperfusion injury)
Prepare to intubate, Monitor co2, Secretions, ABG’s, Turning, mouth care, ROM, Prone positioning, enteral feedings,
Direct Causes of ARDS
Common (Pneumonia, Aspiration of gastric contents) Uncommon (Pulmonary contusion, Near drowning, Inhalation injury, fat embolism, reperfusion injury)
In-diret cause of ARDS
Common (Sepsis, Severe trauma with shock, Multiple transfusion) Uncommon (Post cardiac surgery, Pancreatitis, drug overdose, After massive rransfusion)
Autoimmune Neurologic disorders
Multiple sclerosis, Myasthenia gravis, Duillian- barre syndrome
What is Multiple Sclerosis?
Demyelination disease of the CNS ( destruction of the fatty protein material that surround certain nerve fibers in the brain and spinal cord)
Peak of Multiple sclerosis
25-35 (women) Genetic predisposition, smoking, lack of vit-D, Epsein Barr virus (no cure)
Symptoms of Multiple Sclerosis
Ringing of the ears, blurred vision, dec. hearing, nystagmus, dysphagia, weakness may turn into paralysis, Urinary retention, spastic bladder, constipation, ataxia, vertigo, numbness, bradycardia
Life expectancy for MS
5-7 years.-, frequent remission
Symptom treatment for MS
Interferon b-1a, and interferon b-1b, glatiramer acetate, IV methylprednisolone
Nurse treatment for MS
Emotional support, promote mobility, rest, self care, and promoting sexual function
Assessment for MS
Neurologic deficits, secondary complications, Impact of disease on physical, social, and emotional function and on lifestyle, Patient and family coping
Nrusing diagnosis for MS
Impaired physical mobility, risk for injury, impaired bowel and bladder function, impaired communication, disturbed thought process, ineffective coping, impaired home maitenance, Potential sexual dysfunction
Nursing process of MS Planning
Promote mobility, avoidance of injury, bowel and bladder continence, speech and swallowing mech., improve cognitive function, develop coping strengths, improve home maint.,adapt to sexual dysfunction
Is the following statement true or false? Myasthenia gravis is an autoimmune attack on the peripheral nerve myelin
False, Myoneural junction,
What is myasthenia gravis?
Autoimmune disorder affecting myoneural junction directed at acetylcholine
Symptoms of Myasthenia gravis
Diplopia, and ptosis, weakness of facia muscles caused ny lower neuron lesion, Swallowing and voice impairment (dysphonia), larynheal dysfunction, and dysphagia, weakness in all extremeties and intercostal muscles. (no cure)
Medical management of Myasthenia gravis
Directed at improving function and reducing and removing circulating antibodies, Meds: Anticholinesterase, and immunosuppresive therapy, IV immunoglobulin, plasmapheresis, thymectome
What is acetylcholines involvement in MG?
Decreased binding to the receptor site required for muscular contraction in the thymus gland
Pharmacologic treatment of symptoms
corticosteroids suppress immune response
Nursing process (diagnosis) for MG
Fespiratory failure R/T severe weakness of intercostal muscles
Myasthenic Crisis
Disease exacerbation, or precipitating event (respiratory infection), Severe generalized muscle weakness with respiratory and bulbar weakness, Respiratory compromise or failure
Cholinergic crisis
Over medication with cholinesterase inhibitors, severe muscle weakness with respiratory and bulbar weakness, May develop respiratory compromise and failure
What is dysphonia?
voice impairment or altered voice production
MEdical manegement of MG
Adequate ventilation, intubation and mechanical ventilation may be needed, ABG’s, serum electrolytes, I&O, daily weight, NG feeding may be needed, Avoid sedatives and tranquilizers
What is Guillain-barre syndrome?
Autoimmune disorder with acute attack of peripheral nerve myelin (rapid segmental demyelination of perepherial nerves, and cranial nerves (prepare to intubate)
Symptoms of GBS
dyskanesia (cant execute involuntary movement) Hyporeflexia, and paresthesias (follows viral infection)
Other sx of GBS
weakness, paralysis, paresthesias, pain, and absent reflexes, starting at feet working up, bulbar weakness, cranial nerve sx, tachycardia, bradycardia, hypertension or hypotension
GBS
More frequent in males between 16-25 and over 55. peaks at week 2, but no linger than 4 weeks
Medical management of GBS
Intensive care management, contiuous monitoring, and respiratory support. Complete recovery, Mobility, IV fluids, Parenteral nutrition, bowel sounds, gag reflex, Watch for DVT
Nursing care of GBS DX
ineffective br3eathing pattern, impaired gas exchange, impaired physical mobility, imbalance nutrition, impaired verbal communication, fear, anxiety
Interventions GBS
Physical mobility and prevention of /DVT, limbs in functional position, Passive ROM, Twice daily, frequent repositioning every 2 hours, elastic compression hose, or compression boots, swallowing and gag reflex, Plan for communication, Dec. fear and anxiety, Info and support, refer to support group, relaxation measures, positive attitude and atmosphere, and diversional activities.
What is Muscular dystorphy?
Incurable characterized by progressive weakening and wasting of skeletal and voluntary muscles, genetic (duchenne muscular dystrophy
Symptoms of MD
Muscle wasting and weakness, abnormal elevation in serum levels of muscle enzymes, monitor CPK Mostly males, Dont live to adulthood
Nursing care for MD
supportive care, educate about self care, and continuing care, max level of function. Deformed thorax to secondare or severe scoliosis, Chest infection, atelectasis, pulmonary hypoplasia and ventalitory failure leading causes of death
Simple non-invasive therapy
o2,nebulizer therapy, chest physiotherapy [CPT], breathing retraining
Highly invasive treatments
intubation, mechanical ventilation, surgery
Oxygen Therapy
administering oxygen at a concentration greater than what is in the atmosphere
Reasons for oxygen therapy
hypoxemia, decrease in the arterial oxygen tension in the blood. Hypoxia- decrease in oxygen perfusion to the tissues and cells.
symptoms that cause need for oxygen therapy
fatigue, drowsiness, apathy, inattentiveness, and delayed reaction time may occur
Oxyen
Is a medication and should be prescribed by a doctor unless it’s an emergency situation (2ml/dl)
subtle indicators of inadequate oxygenation when oxygen is given by any method
confusion, restlessness progressing to lethargy, diaphoresis, pallor, tachycardia, tachypnea, and hypertension.
Oxygen Toxicity
may occur when too high concentration of oxygen (greater than 50%) is given for an extended period (generally longer than 24 hours
Signs and symptoms of oxygen toxicity
substernal discomfort, paresthesias, dyspnea, restlessness, fatigue, malaise, progressive respiratory difficulty, refractory hypoxemia, alveolar atelectasis, and alveolar infiltrates evident
Absorption Atelectasis
adverse effect of the administration of high concentrations of oxygen (greater than 50%) to patients who are sedated and breathing small tidal volumes of air (volume of air inspired and expired with each breath
Devises of oxygen administration
Cannula
1—2 3–5 6 24–28 32–40 44 Lightweight, comfortable, inexpensive, continuous use with meals and activity
Easily dislodged, from nares, skin breakdown over ears or nares, nasal mucosal drying, variable FiO2
Devises of oxygen administration, low
Nasal catheter, Flow rate of 1-6, o2 percentage 24-44, Inexpensive, does not require a tracheostomy. Can cause.
Nasal mucosa irritation; catheter should be changed frequently to alternate nostril
Devices of oxygen administration, low
simple mask, 5-8l/m, o2% 40-60, Simple to use, inexpensive
Complications, Poor fitting, variable FiO2, must remove to eat
Partial rebreathing mask, low, have a reservoir bag that must remain inflated during both inspiration and expiration, the first third of the exhalation fills the reservoir bag.
8-11, o2% 50-75, Moderate O2 concentration
Warm, poorly fitting, must remove to eat
Non-rebreathing mask, low, A one-way valve located between the reservoir bag and the base of the mask allows gas from the reservoir bag to enter the mask on inhalation but prevents gas in the mask from flowing back into the reservoir bag during exhalation
10-15, o2% 80-95, High O2 concentration
Poorly fitting, must remove to eat
Transtracheal catheter high flow, insert a catheter through a small incision directly into the trachea. It is indicated for patients with chronic oxygen therapy needs
1/4-4, 60-100, More comfortable, concealed by clothing, less oxygen liters per minute needed than nasal cannula
Requires frequent and regular cleaning, requires surgical intervention, with associated risk for surgical complications
Mask, Venturi, high flow, most reliable and accurate method for delivering precise concentrations of oxygen through noninvasive means.
(4-6, 24,26,28), (6-8, 30,35,40)Provides low levels of supplemental O2
Must remove to eat
Precise FiO2, additional
Mask, aerosol, high flow
8*10, 30-100, Good humidity, accurate FiO2
Uncomfortable for some
Tracheostomy collar, high flow
8-10, 30-100,
Good humidity, comfortable, fairly accurate FiO2
T-piece, high flow, onnects to the endotracheal or tracheostomy tube and is useful in weaning patients from mechanical ventilation
8-10, 30-100, Same as tracheostomy collar
Heavy with tubing
Face tent, high flow
8-10,30-100, Good humidity, fairly accurate FiO2
Bulky and cumbersome
Oxygen-Conserving Devices, Pulse dose (or demand)
10-40ml/breath, Deliver O2 only on inspiration, conserve 50–75% of O2 used
Must carefully evaluate function individually
low-flow (variable performance)
the patient breathes some room air along with the oxygen
high-flow (fixed performance)
provide the total inspired air. A specific percentage of oxygen is delivered independent of the patient’s breathing. High-flow systems are indicated for patients who require a constant and precise amount of oxygen.
Hyperbaric oxygen therapy
treat conditions such as decompression sickness, air embolism, carbon monoxide poisoning, cyanide poisoning, smoke inhalation, gangrene, tissue necrosis, wound healing, skin grafts, refractory anaerobic infections, and refractory osteomyelitis , 100% o2
Patient teaching for oxygen therapy
patient is instructed to see their primary provider every 6 months or more often, if indicated. Arterial blood gas measurements and laboratory tests are repeated annually or more often if the patient’s condition changes.
Incentive spirometry
method of deep breathing that provides visual feedback to encourage the patient to inhale slowly and deeply to maximize lung inflation and prevent or reduce atelectasis. The purpose of an incentive spirometer is to ensure that the volume of air inhaled is increased gradually as the patient takes deeper and deeper breaths.
volume type, incentive spir
the tidal volume is set using the manufacturer’s instructions. The patient takes a deep breath through the mouthpiece, pauses at peak lung inflation, and then relaxes and exhales. Taking several normal breaths before attempting another with the incentive spirometer helps avoid fatigue. The volume is periodically increased as tolerated.
flow type, incentive spir
olume is not preset. The spirometer contains a number of movable balls that are pushed up by the force of the breath and held suspended in the air while the patient inhales. The amount of air inhaled and the flow of the air are estimated by how long and how high the balls are suspended.
Indications
Incentive spiro use
Incentive spirometry is used after surgery, especially thoracic and abdominal surgery, to promote the expansion of the alveoli and to prevent or treat atelectasis.
Nursing managemet for Incentive spiro
placing the patient in the proper position, educating the patient on the technique for using the incentive spirometer, setting realistic goals for the patient, and recording the results of the therapy (see Chart 21-3). Ideally, the patient assumes a sitting or semi-Fowler’s position to enhance diaphragmatic excursion; however, this procedure may be performed with the patient in any position.
Chest physiotherapy (CPT
postural drainage, chest percussion and vibration, and breathing retraining. In addition, educating the patient about effective coughing technique is an important part of CPT. The goals of CPT are to remove bronchial secretions, improve ventilation, and increase the efficiency of the respiratory muscles
Endotracheal intubation
The oral route is preferred since oral intubation is associated with less trauma and lesser rates of infection; furthermore, the oral route can typically accommodate a larger diameter
