Week 6; Acute Care Respiratory Flashcards
(143 cards)
1
Q
ARDS
A
Characterized by rapid onset of noncardiac pulmonary edema, progressive refractory hypoxemia, extensive lung tissue inflammation, small blood vessel injury, multisystem organ malfunction, and varied initial admitting diagnoses.
2
Q
ARDS is caused by
A
acute lung injury from unregulated systemic inflammatory response to acute injury or inflammation
3
Q
ARDS patho after acute lung injury
A
Damaged capillary membranes → plasma, blood cells leak into interstitial space
Damage to alveolar membrane → fluid enters alveoli
Dilutes, inactivates surfactant → damage to surfactant-producing cells
Deficit of surfactant, increased alveolar surface tension, alveolar collapse with atelectasis
Lungs become less compliant, gas exchange impaired
Hyaline membranes form → further reduced gas exchange, compliance
Fibrotic changes in lungs → less surface area for gas exchange
Hypoxemia becomes resistant to improvement with supplemental O2
PaCO2 rises as diffusion further impaired
4
Q
ARDS causes
A
Hypoxemia, metabolic acidosis, sepsis, multiple organ system dysfunction
5
Q
ARDS risk factors
A
Greater for men than women
Greater for African Americans
Patients who develop ARDS from sepsis have poorer outcomes than those who develop ARDS from pulmonary infections or trauma
6
Q
Direct insults that can cause ARDS
A
Pulmonary infections
Aspiration of gastric contents
Inhalation injuries
Smoke inhalation
Saltwater inhalation
7
Q
Indirect insults that can cause ARDS
A
Overall body sepsis
Trauma
Gastrointestinal (GI) infections
Drug overdose
Multiple blood transfusions
8
Q
ARDS s/s
A
Dyspnea and tachypnea are early signs
Chest x-ray, arterial blood gases (ABGs) often normal
Respiratory rate, intercostal retractions, use of accessory muscles of respiration increase
Tachypnea
Rales, rhonchi develop
Chest x-ray shows interstitial changes, patchy infiltrates
Pulse oximetry, ABG levels show refractory hypoxemia
Agitation, confusion, and lethargy
9
Q
Nurse’s focus for the pt with ARDS
A
Constantly monitor patient’s condition, respond to subtle cues indicating changes, and intervene appropriately
10
Q
ARDS dx tests
A
ABG analysis to determine O2 levels in blood, chest x-ray or chest CT to determine fluid in lungs, CBC, blood chemistry, blood cultures to help find cause of ARDS, and sputum culture to determine cause of infection
11
Q
Pharmacologic therapy for ARDS
A
No definitive drug therapy for ARDS
Nitric oxide reduces intrapulmonary shunting and improves oxygenation
Surfactant therapy
Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are being studied
Corticosteroids may be used late in disease course when fibrotic changes occur to improve oxygenation, lung mechanics
12
Q
Mainstay of ARDS management
A
Endotracheal intubation, rarely possible to maintain adequate oxygenation with O2 therapy alone. Mechanical ventilation does not cure ARDS
Supports respiratory function while underlying problem is found, treated
13
Q
Vent support complications
A
Ventilator-associated pneumonia (VAP), barotrauma, pneumothorax, cardiovascular effects, GI effects
14
Q
Negative pressure ventilators
A
Create negative pressure externally to draw chest outward and air into lungs
15
Q
Positive pressure ventilators
A
Push air into lungs, used more often than negative pressure ventilators
16
Q
Noninvasive positive pressure ventilation (NIPPV)
A
Tight-fitting face mask, nasal mask, nasal shield, or nasal pillows, may prevent need for tracheal intubation. Ventilatory support for patients with sleep apnea, neuromuscular disease, or impending respiratory failure.
17
Q
Weaning from ventilator support
A
When underlying process causing respiratory failure is corrected or stabilized. Process and time required depend on several factors:
Preexisting lung condition
Duration of mechanical ventilation
Patient’s general physical and psychologic condition
Vital signs, respiratory rate, extent of dyspnea, blood gases, clinical status used to evaluate weaning and its progress
T-piece, CPAP may be used for weaning
SIMV, PSV
When duration of ventilation long enough that respiratory muscles need to be reconditioned
Weaning is a primary use for PSV
18
Q
Terminal weaning:
A
when survival without assisted ventilation is not expected
19
Q
Artificial airways
A
Inserted to maintain patent air passage
20
Q
Oropharyngeal airways
A
Stimulate gag reflex, used only for semiconscious, unconscious patients
21
Q
Nasopharyngeal airways
A
Usually well tolerated by alert patients, frequent oral and nares care needed
22
Q
Endotracheal tubes
A
In patients under general anesthesia or in emergency situations. Insertion requires specialized education, patient unable to speak while tube in place
23
Q
Tracheostomies
A
For long-term airway support, opening into trachea through neck
Open surgical method: done in operating room
Percutaneous method: can be done at bedside in critical care unit
Nursing care: maintain airway patency and precautions to provide humidity
24
Q
Swan-Ganz catheter
A
Monitor pulmonary artery pressures and cardiac output
25
Arterial line
Repeated blood gas analysis and continuous arterial pressure monitoring
26
Nutrition and fluids for pt with ARDS
Serum electrolytes drawn frequently, monitor intake and output (I&O), daily weight, fluid and electrolyte status, enteral or parenteral nutrition during mechanical ventilation, jejunostomy tube may be used to reduce risk of regurgitation, aspiration
27
ARDS nursing cares
Prone positioning in conjunction with mechanical ventilation, treatment of any infection with IV antibiotic therapy, correction of underlying condition, careful fluid replacement, low-molecular-weight heparin to prevent thrombophlebitis, pulmonary embolus and DIC
28
Possible ARDS complications
Thrombophlebitis, pulmonary embolus, DIC
29
Children and ARDS
Low incidence, may be underdiagnosed. Immunocompromised children at increased risk
Clinical guidelines reflect differences between adult, pediatric patients: more compliant chest walls in children, higher sedation requirements, baseline airway resistance
Lower hematocrit, functional residual capacity
Lungs not yet fully developed
Advise against routine use of inhaled nitric oxide (NO), exogenous surfactant, corticosteroids, prone positioning. Intubation to be used only in patients who do not respond to other measures or have worsening signs, symptoms
30
Pregnant women and ARDS
Low incidence rates but devastating results; maternal mortality rate as high as 44%
Common obstetric causes: preeclampsia, amniotic fluid embolism, obstetric hemorrhage, sepsis from infection of uterus, fetal membranes, kidneys, influenza during pregnancy.
Goals: adequate ventilation, nutritional support
Prone positioning but with caution during third trimester, close fetal monitoring
31
Older adults and ARDS
Greater risk than rest of adult population, especially over age 40
Due partly to age-related changes in respiratory physiology, higher mortality rate. Less likely to receive same intensity of care as other ARDS patients. Significantly more likely to die from multiple organ failure, other complications. Treatments aimed at prevention of nonpulmonary organ complications help improve overall outcomes. Adequate nutrition contributes to improved O2 levels, lung function, diet high in omega-3 and -6 fatty acids
32
Nursing process with ARDS
Careful, continuous monitoring of airway, breathing, circulation, monitor for changes in level of consciousness (LOC), oxygenation, perfusion require rapid intervention.
33
Assessment of the patient with ARDS
Respiratory rate, rhythm, auscultation of lungs, LOC, including orientation, baseline vital signs, peripheral perfusion
34
In the pt with ARDS, monitor
Vital signs hourly, oxygenation status with ABG, pulse oximetry, neurologic status, including orientation and LOC, lung and heart sounds
35
Interventions for the pt with ARDS
Analgesia, anxiolytics, sedation, provide beta-agonist to maintain patent airways, maintain head of bed at 30 degrees or higher, prone position as tolerated 3–4x/day, suction airways as needed, monitor hemodynamic status with central venous catheters or pulmonary artery catheter as ordered, monitor renal function by I&O, blood urea nitrogen (BUN) and creatinine levels, foley, IV fluids as needed but avoid fluid overload, monitor glucose levels, maintain within normal limits
36
Maintaining a patent airway in the pt with ARDS
Perform postural drainage (PVD) as ordered, assess fluid balance, maintain adequate hydration, suction as needed, obtain sputum for culture if sputum appears purulent or is odorous, secure endotracheal or tracheostomy tube with adequate slack on tubing, restrain patient’s hands if necessary
37
Promote spontaneous ventilation in the pt with ARDS
Place patient in Fowler or high-Fowler position, minimize activities, energy expenditures, assist with activities of daily living (ADLs), space procedures, activities, allow uninterrupted periods of rest, assess, document respiratory rate, VS, O2 saturation every 15–30 minutes, promptly report worsening data, administer O2 as ordered, monitor response
38
Enhance cardiac output in the pt with ARDS
Assess LOC at least every 4 hours, monitor pulmonary artery pressure, central venous pressure, cardiac output every 1–4 hours, assess heart and lung sounds frequently, weigh daily at same time, provide frequent skin care, maintain IV fluids as ordered, administer analgesics, sedatives, neuromuscular blockers as ordered
39
Interventions for dysfunctional ventilatory weaning response
Assess vital signs every 15–30 minutes
Place in Fowler or high-Fowler position
Explain weaning procedures, expected changes in breathing
Remain with patient during initial periods following changes of setting
Limit procedures, activities during weaning periods
Provide diversion
Begin weaning in morning
May discontinue overnight to provide rest
When SIMV used for weaning, decrease rate by increments of 2 breaths/min
Avoid drugs that may depress respiratory
Keep oxygen at bedside
Provide pulmonary hygiene
40
ARDS teaching
Need to tailor activities until maximal respiratory function returns, avoid smoking, exposure to smoke and other pollutants, immunizations for pneumonia, influenza
41
Cystic fibrosis:
Inherited disorder that affects secretory glands, particularly glands responsible for secreting mucus, digestive enzymes, sweat (exocrine glands). In turn, affects lungs, sinuses, digestive organs, reproductive organs.
42
CF patho
CF stems from mutation of CFTR gene. This protein is central to movement of chloride into, out of body cells. Mutation affects movement of salt and water into, out of cells. Entry of too much salt, not enough water causes production of thick, sticky mucus that obstructs ducts and passageway, including airways, pancreatic duct. Causes airway occlusion and creates environment that supports bacterial growth. Immune response causes WBCs to release sticky chemical substances into mucus. This worsens obstruction and exacerbates inflammation, infection. Often diagnosed before 2 years of age, but manifestations vary, may occur later
43
CF prevention
Genetic testing
44
CF clinical manifestations: hallmark and respiratory
Increased level of chloride in sweat: hallmark manifestation
Respiratory manifestations include chronic cough, chronic sinusitis, recurrent infection, including bronchiectasis, pneumonia
Recurrent respiratory infections → scar tissue, cysts in lungs
Pneumothorax in later stages of disease
Pulmonary damage may lead to respiratory failure and death
45
Other s/s of CF
Chronic diarrhea, nutritional deficiencies, obstruction of pancreatic ducts, impaired production of enzymes needed for food digestion, malnutrition, delays in growth and development, impaired insulin production, impaired blood glucose control, blockage and inflammation of bile duct, hepatic dysfunction, gallstones, Men with CF absence of vas deferens, obstruction and impaired development of vas deferens, fertility treatment or surgical procedures may be needed, women with CF have decreased fertility, changes of pregnancy may exacerbate effects of CF
46
CF dx tests
Prenatal screening: if mother has abnormal CFTR gene, father is tested, if both parents are carriers, fetus may be tested
Amniocentesis: chorionic villus sampling, newborns screened at birth in United States
Sweat test: older children or adults may be tested if they show warning signs, such as:
Bronchiectasis
Chronic lung or sinus infections
Nasal polyps
Pancreatitis
Male infertility
47
Surgery for CF
Removal of nasal polyps to improve breathing, removal of mucus via endoscopic lavage to improve breathing, oxygen therapy for advanced lung disease, feeding tube insertion to administer additional nutrients, bowel surgery in case of bowel blockage or intussusception
48
Pharmacologic therapy for CF
Bronchodilators for patients with mild disease for specific purposes
Mucolytics, antibiotics, CFTR modulators, vaccination, anti-inflammatory drugs, digestive drugs, including vitamin and mineral supplements
49
CFTR modulators
Revolutionary treatment targeting cause of problem, patients age ≥12 with two copies of most common mutation. Relatively new, may be prohibitively expensive
50
Nonpharmacologic therapy for CF
Airway clearance techniques such as coughing, huffing, chest physical therapy, percussion, vibration, deep breathing, pulmonary rehabilitation, lifestyle interventions, healthy, well-balanced diet, high fluid intake, regular exercise, fitness training, refraining from smoking, avoiding secondhand smoke, good hygiene, coughing into tissue, disposing immediately, cleaning hands afterward
51
Children and infants CF considerations
Prenatal indicators of CF: prenatal testing, hyperechoic or echogenic bowel on ultrasound
Neonates: meconium ileus
Children: intussusception, poor weight gain, delayed growth and development, failure to thrive, respiratory difficulties
Vigilant assessment, monitoring of airway patency, respiratory status required to protect safety of neonatal, pediatric patients
Staying up to date on immunizations is critical
52
Children and infants CF considerations
Prenatal indicators of CF: prenatal testing, hyperechoic or echogenic bowel on ultrasound
Neonates: meconium ileus
Children: intussusception, poor weight gain, delayed growth and development, failure to thrive, respiratory difficulties
Vigilant assessment, monitoring of airway patency, respiratory status required to protect safety of neonatal, pediatric patients
Staying up to date on immunizations is critical
53
CF in adolescence
Continue to require CPT, enzymes, vaccines, other medications
Nutritional supplementation: extra calcium, vitamin D
Puberty may be delayed, teens can live normally as long as they engage in appropriate self-care, adequate nutrition and sleep, scheduling provider appointments, managing medication regimens, healthcare decisions, parents should encourage autonomy while providing emotional, social support. Adolescents should be encouraged to think about future education, career plans
54
CF in adults
Long-term damage to lungs, pancreas, liver → organ transplantation may be needed
Surgery may be needed to promote normal bowel function, proper sinus drainage
Kegel exercises to strengthen pelvic floor muscles
Women: normal fertility rates if get adequate nutrition, have good lung function
Men: only 2–3% are fertile
Intracytoplasmic sperm injection to help partner conceive. Sperm extracted, used for in vitro fertilization
55
CF in pregnant women
Outcome of pregnancy for woman with CF depends heavily on respiratory health
Good lung function = less likely to experience preterm delivery
Lower than average weight gain during pregnancy
Nutritional supplementation often necessary
Higher risk of gestational diabetes
Therapeutic regimen might need to be changed
Some drugs may need to be discontinued until postpartum period
56
Promote effective breathing for the pt with CF
Teach patient to call primary care provider if pulmonary exacerbation occurs
Administer bronchodilators before beginning airway clearance techniques or administering inhaled mucolytics
Teach patient to use incentive spirometer
Administer pure O2 as prescribed
57
Promote effective breathing for the pt with CF
Teach patient to call primary care provider if pulmonary exacerbation occurs
Administer bronchodilators before beginning airway clearance techniques or administering inhaled mucolytics
Teach patient to use incentive spirometer
Administer pure O2 as prescribed
58
Promote airway clearance in the pt with CF
Teach patient airway clearance techniques
Administer mucolytics before beginning CPT
Assist patient with CPT
Teach patient, caregivers how to perform CPT
During exacerbations, CPT should be administered more often
Up to 4 times/day for 1 hour per session in severe exacerbation
59
Control and prevent infection in the pt with CF
Teach patient how to self-administer inhaled antibiotics
Teach patient importance of vaccinations, including influenza
Teach patient and caregiver hand hygiene techniques
Teach patient proper respiratory hygiene
Teach patient to avoid close contact with other individuals with CF
Drug-resistant and virulent pathogens can pass more easily
Use proper infection control techniques when caring for patients with CF
60
Monitor nutrition status in the pt with CF
Advocate for nasogastric or gastronomy tube feedings if necessary
Teach patient with feeding tube how to administer feedings, care for equipment
This includes caregivers
Assess for patient adherence to nutrition plan
Make referrals to nutritionist or dietitian as needed
Provide patient teaching about appropriate nutrition intake
Caloric intake may need to be increased during pulmonary exacerbations
Monitor patient for signs of electrolyte or fluid imbalance
Especially hyponatremia, hypochloremia, dehydration
61
Metabolic acidosis
Characterized by low pH (<7.35)
Low bicarbonate (<22 mEq/L)
May be caused by excess acid in body, loss of bicarbonate from body. Respiratory system attempts to return pH to normal
62
Four basic mechanisms may cause metabolic acidosis
Accumulation of metabolic acids, excess loss of bicarbonate, increase in chloride levels, fluid imbalance
63
Excess metabolic acids causes
Excess acid production, impaired renal elimination of metabolic acids, toxic substances may break down into acid products or stimulate metabolic acid production, increase H+ concentration of body fluids, buffering by bicarbonate → high anion gap acidosis
64
Excess loss of bicarbonate through
Intestinal suction, severe diarrhea, ileostomy drainage, fistulas
65
Electrolytes and metabolic acidosis
Potassium retained
Calcium released from plasma proteins
Magnesium levels may fall
66
Etiology of metabolic acidosis
Metabolic acidosis usually develops during course of another disease, such as tissue hypoxia from shock or cardiac arrest, type 1 diabetes mellitus, acute or chronic renal failure, diarrhea, intestinal suction, abdominal fistulas, ingestion of acidic substance or one that can be metabolized to acid
67
Metabolic acidosis risk factors
DKA
Renal failure
Severe sepsis
Salicylate intoxication
Severe diarrhea
Eating disorders involving laxative abuse, severe diet restriction
68
Metabolic acidosis s/s
REMEMBER, as the PH goes, so goes my patient! Kaussmaul respirations
69
Metabolic acidosis treatment: Alkalinizing solution
If pH < 7.1
Sodium bicarbonate most common
Lactate, citrate, acetate solutions also used
Given IV for severe acute acidosis
Oral route for chronic acidosis
70
DKA treatment
IV insulin, fluid replacement
71
Alcoholic ketoacidosis treatment
Saline solutions, glucose
72
Lactic acidosis treatment
Correct underlying problem
Improve tissue perfusion
73
Children and metabolic acidosis
More likely to develop metabolic acidosis from bicarbonate loss through diarrhea
Congenital or acquired renal tubular acidosis → large loss of bicarbonate, with or without potassium depletion
74
Older adults and metabolic acidosis
Higher concentration of H+ in metabolic acidosis
Medications may affect acid–base balance
75
Nursing considerations for metabolic acidosis
Monitor for fluid volume excess, reduce risk for injury,
76
Metabolic alkalosis
Characterized by high pH (>7.45)
High bicarbonate (>28 mEq/L)
May be caused by loss of acid or excess bicarbonate in body, respiratory system attempts to compensate
PaCO2 increases (>45 mmHg)
77
Metabolic alkalosis patho
Hydrogen ions lost through kidneys, gastric secretions, or shift of H+ into cells
Loss of hydrogen ions from vomiting, gastric suction
Increased renal excretion prompted by hypokalemia
Excess bicarbonate from ingesting antacids or overtreatment of metabolic acidosis
More calcium combines with serum proteins, reducing ionized serum calcium
Affects potassium balance, can cause hypokalemia
High pH depresses respiratory system as CO2 is retained to restore carbonic acid–bicarbonate ratio
78
Metabolic alkalosis etiology
Excessive ingestion of antacids
Excessive use of bicarbonate
Lactate administration in hemodialysis
Hyperaldosteronism
Hypokalemia
Hypochloremia
Nasogastric suctioning
Loop diuretics
79
Metabolic alkalosis risk factors
Rarely occurs as primary disorder
Risk factors include
Hospitalization
Hypokalemia
Treatment with bicarbonate
Older adults → delicate fluid/electrolyte balance
Self-induced vomiting
Chronic hypercapnia respiratory failure
80
S/S of decreased calcium ionization (met. alk.)
Numbness/tingling around mouth, fingers, toes
Dizziness
Trousseau sign
Muscle spasms
Respirations depressed
Respiratory failure with hypoxemia
Respiratory acidosis
81
ABG in met. alk.
Show pH >7.45
Bicarbonate level >26 mEq/L
82
Electrolytes in met. alk.
Serum electrolytes
Decreased serum potassium <3.5 mEq/L
Decreased chloride <95 mEq/L
Urine pH may be low
ECG pattern shows changes similar to those seen with hypokalemia
83
Pharmacologic therapy for met. alk.
Restore normal fluid volume
Administer potassium chloride solution
Administer sodium chloride solution
Severe alkalosis → administer acidifying solution
Drugs may also be used to treat underlying cause of alkalosis
84
Teaching for met. alk.
Teach risks of using sodium bicarbonate
Availability of other antacid preparations
Seek medical evaluations for persistent gastric symptoms
In hospital setting, monitor lab values carefully, particularly patients undergoing continuous gastric suction
Teach about
Using appropriate antacids
Using potassium supplements as ordered
Contacting primary care provider if uncontrolled or extended vomiting develops
85
Nursing considerations for met. alk
Monitor for impaired gas exchange, fluid volume deficit
86
Diarrhea =
Vomiting =
Acidosis
Alkalosis
87
Respiratory acidosis
Caused by excess of carbonic acid
Characterized by a pH <7.35
PaCO2 >45 mmHg
May be acute or chronic
In chronic respiratory acidosis, bicarbonate is >26 mEq/L
Kidneys compensate by retaining bicarbonate
88
Respiratory acidosis patho and etiology
Both acute and chronic respiratory acidosis result from CO2 retention
Caused by alveolar hypoventilation
Hypoxemia frequently accompanies respiratory acidosis
89
Acute respiratory acidosis results from sudden failure of ventilation, such as:
Chest trauma
Aspiration of foreign body
Acute pneumonia
Overdose of narcotics or sedatives
PaCO2 rises rapidly
pH falls markedly
pH ≤7 can occur within minutes
Hypercapnia
90
Chronic respiratory acidosis
Associated with chronic respiratory or neuromuscular conditions that affect alveolar ventilation
Majority have COPD → bronchitis, emphysema
PaCO2 increases over time, remains high
Kidneys retain bicarbonate
pH often close to normal
Acute hypercapnia may not develop when CO2 levels rise gradually
Risk of carbon dioxide narcosis
91
Respiratory acidosis risk factors
Acute lung disease
Chronic lung disease
Trauma
Narcotic analgesics
Airway obstruction
Neuromuscular disease
92
S/s of hypercapnia
Cerebral vasodilation
LOC progressively decreases
Rapid changes in ABGs
Skin warm, flushed
Pulse elevated
93
ABG's dx for respiratory acidosis
pH <7.35
PaCO2 >45 mmHg
94
Respiratory acidosis bicarb
Increases to >26 mEq/L if condition persists
95
Chronic respiratory acidosis
PaCO2 may be significantly elevated
HCO3 may be significantly elevated
96
Pharmacologic therapy for respiratory acidosis
Bronchodilator drugs
Antibiotics for respiratory infections
Narcotic antagonists
97
Metabolic acidosis respiratory support
Focus on improving alveolar ventilation, gas exchange
Severe acidosis and hypoxemia
Intubation and mechanical ventilation
PaCO2 level lowered slowly
O2 administered cautiously
Pulmonary hygiene
Adequate hydration
98
Metabolic acidosis risk factors for children
Risk factors
Asthma
Pneumonia
Airway obstruction
Acute pulmonary edema
ARDS
Head trauma
Poisoning
99
Metabolic acidosis risk factors for older adults
Risk factors
COPD
Chest wall abnormalities
Pneumonia
Respiratory muscle weakness
HCO3 retention by kidneys in compensation for CO2 retention from hypoventilation
Outcome depends on nature of illness, early diagnosis/treatment
100
Metabolic acidosis teaching for parents
Children with asthma, airway obstruction, influenza, and pneumonia are at risk
Teach parents prevention methods
Deep breathing (several times/day)
Signs of infection
Positioning to facilitate chest expansion
Medication administration (as appropriate)
Use of ordered devices (e.g., home respirators, nebulizers)
101
Respiratory alkalosis
Characterized by a pH >7.45
PaCO2 <35 mmHg
Always caused by hyperventilation, leading to carbon dioxide deficit
102
Acute respiratory alkalosis
pH rises rapidly as PaCO2 falls
Kidneys unable to adapt rapidly → bicarbonate level remains in normal limits
103
Respiratory alkalosis causes
Anxiety-based hyperventilation is most common cause
Other causes of hyperventilation: high fever, hypoxia, gram-negative bacteremia, thyrotoxicosis, aspirin overdose, anesthesia, mechanical ventilation
104
Chronic respiratory alkalosis
Kidneys compensate → eliminate bicarbonate
Restore ratio of bicarbonate to carbonic acid
Bicarbonate level is lower than normal
pH may be close to normal range
105
Results of alkalosis
Increases binding of extracellular calcium to albumin
Reduces ionized calcium levels
Neuromuscular excitability increases
Manifestations similar to hypocalcemia develop
Low CO2 levels cause vasoconstriction of cerebral vessels
106
Respiratory alkalosis risk factors
Anxiety disorders
Mechanical ventilation settings
Breaths per minute too high
Peak pressures too high
107
Respiratory alkalosis s/s
Light-headedness
Feeling of panic and difficulty concentrating
Circumoral and distal extremity paresthesias
Tremors
Positive Chvostek sign
Trousseau sign
Tinnitus
Sensation of chest tightness, palpitations
Seizures and loss of consciousness
108
Respiratory alkalosis ABG
Show pH >7.45
PaCO2 <35 mmHg
109
Chronic hyperventilation bicarb
Serum bicarbonate <22 mEq/L
110
Respiratory alkalosis treatment
Management focuses on correcting the imbalance and treating underlying cause
Create calm environmental
Quiet, low stimulation
Reduce anxiety or panic
ABGs prior to meds or O2 therapy
Antianxiety agent
Relieve anxiety
Restore normal breathing pattern
Additional medications to correct underlying problems
111
Paper bags and respiratory alkalosis
Historically recommended
Will help raise CO2 levels but can cause hypoxia
Not useful in other disease that mimic hyperventilation
Elevated CO2 can trigger panic attacks, worsening hyperventilation
112
Respiratory alkalosis teaching
Best treatment → teach breathing exercises
Patient should take slow, regular breaths
Patient should breathe into cupped hands
Encourage stress reduction
113
Respiratory alkalosis nursing care focused on
Reducing anxiety through environmental manipulation
Restful environment to help patients breathe slowly and effectively
114
Respiratory alkalosis nursing interventions include
Assess respiratory rate, depth, and ease
Monitor vital signs and skin color
Obtain subjective assessment data
Circumstances leading to current situation
Current health and recent illnesses
Medication use
Current manifestations
Reassure patient that this is not a heart attack
Instruct patient to maintain eye contact and breathe with nurse to slow respiratory rate
Protect patient from injury
Refer for counseling
115
Respiratory alkalosis planning and teaching
directed toward underlying cause of hyperventilation
Discuss anxiety and stress management strategies
Teach patient how to identify a hyperventilation reaction
Teach patient to provide self-care
Teach patient when to seek medical intervention
116
S/S of pulmonary edema
Crackles, dyspnea at rest, disorientation or acute
confusion, tachycardia, hyper or hypotension, decreased urine output, cough with frothy, pink
sputum, anxiety/restlessness, lethargy
117
Causes of pulmonary edema
Associated with CKD, associated with heart failure, neurogenic pulmonary edema, high Altitude pulmonary edema
118
Managing pulmonary edema
Immediate objective is to improve oxygenation and improve
pulmonary congestion. Find and treat the underlying cause
119
Managing pulmonary edema: MAD DOG
* M-Morphine
* A- Airway
* D-Decrease preload (NTG)
* D-Diuretics (Lasix)
* O-Oxygen
* G-Blood Gases (ABG)
120
Pulmonary edema nursing interventions
Positioning: High Fowler’s HOB at 90 degrees
O2 and meds as ordered
Decrease anxiety
Assessment/reassess lungs, SaO2, electrolytes
I&O, daily weight, oral care, edema, pt/family education and support
121
Pulmonary embolus (PE)
A PE can arise from anywhere in the body, but most
commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets and at
other sites of presumed venous stasis.
122
PE risk factors
*Prolonged immobilization
* Central venous catheters
* Surgery
* Obesity
* Advancing age
* Conditions that increase blood clotting
* History of thromboembolism (DVT)
123
PE prevention
Passive and active range-of-motion exercises for the
extremities of immobilized and postoperative patients
* Ambulate
* Anti-embolism and pneumatic
compression stockings
* Avoid constrictive clothing
* Position changes q 2 hrs
* Low dose anticoagulants
124
Classic s/s of PE
* Dyspnea, sudden onset
* Sharp, stabbing chest pain
* Apprehension, restlessness
* Feeling of impending doom/anxiety
* Cough
* Hemoptysis
*Tachypnea
* Crackles
* Pleural friction rub
* Tachycardia
* S3 or S4 heart sound
* Diaphoresis
* Fever, low-grade
* Petechiae over chest and axillae
* Decreased arterial oxygen saturation (SaO2
125
Nursing interventions for PE
* Oxygen therapy (nasal cannula, mask)
* Reassure patient to decrease anxiety
* High Fowler’s position
* Continuous patient monitoring & assessment
* Ensure adequate venous access
* Continuous monitoring of pulse oximetry
* Bleeding precautions
* Ensure tests are done in timely manner (CBC, PT, PTT, D-Dimer, ABG)
* Drug therapy*
Anticoagulants
Administering anticoagulation (heparin) or fibrinolytic therapy (alteplase tPA) (Chart 32-4)
* Monitoring patient response
* Psychosocial support
126
Surgical management of PE
Embolectomy or inferior vena cava filtration
127
Acute respiratory failure ABG's
* PaO2 <60 mm Hg
* SaO2 <90%; or PaCO2 >50 mm Hg with pH <7.30
* Ventilatory/oxygenation failure
* Patient is always hypoxemic
128
Ventilatory failure
Physical problem of lungs or chest wall
* Defect in respiratory control center in brain
* Poor function of respiratory muscles, especially diaphragm
* Extrapulmonary causes
* Intrapulmonary causes
129
Extrapulmonary causes of ventilatory failure
Muscular disorders: myasthenia gravis, guillain-Barré syndrome, poliomyelitis, spinal cord injuries affecting nerves to intercostal muscles
Central nervous system dysfunction: stroke, increased intracranial pressure, meningitis, opioid analgesics, sedatives, anesthetics, kyphoscoliosis, massive obesity, sleep apnea, external obstruction/constriction
130
Intrapulmonary causes of ventilatory failure
Airway disease: COPD, asthma
Ventilation-perfusion (V̇/Q̇)mismatch:
Pulmonary embolism
Pneumothorax
Acute respiratory distress
syndrome (ARDS)
Amyloidosis
Pulmonary edema
Interstitial fibrosis
131
Common causes of oxygenation failure
Low atmospheric oxygen concentration:
* High altitudes, closed spaces, smoke inhalation, carbon monoxide poisoning
* Pneumonia
* Congestive heart failure with pulmonary edema
* Pulmonary embolism (PE)
* Acute respiratory distress syndrome (ARDS)
* Interstitial pneumonitis-fibrosis
* Abnormal hemoglobin
* Hypovolemic shock
* Hypoventilation
132
Complications of nitroprusside therapy:
Thiocyanate toxicity, methemoglobinemia
133
Combined Ventilatory and oxygenation Failure
Often occurs in patients with abnormal lungs
* Chronic bronchitis
* Emphysema
* Asthma attack
* Diseased bronchioles and alveoli cause oxygenation failure; work of
breathing increases; respiratory muscles unable to function
effectively
134
Interventions for respiratory failure
O2, may need mechanical ventilation, nebulized bronchodilators, corticosteroids?, analgesics, other based on causative factor.. Positioning, relaxation, TCDB
135
Why is mechanical ventilation used?
Used to overcome dangers of
respiratory insufficiency
* Forced oxygen into lungs to
increase the expiration of CO2
* Allows well-distributed airflow
to the alveoli
* Patient’s breathing efforts and
energy expenditure are
decreased
* Improves effectiveness of
coughing and assists with the
expulsion of secretions
136
Nursing care for ET tubes
Assess tube placement, minimal cuff leak, breath sounds, chest wall
movement
* Prevent movement of tube by patient
* Check pilot balloon
* Soft wrist restraints
* Mechanical sedation
137
Endotracheal tube(nose or mouth to
trachea) care
* Assess for bilateral breath
sounds and bilateral chest
expansion
* Mark tube at level it touches
mouth/nose
* Secure with tape to stabilize
138
Trach care
* Cuff is used to prevent aspiration and facilitate mechanical ventilation
* Maintain cuff pressure at 14-20 mm Hg
* Encourage fluids to facilitate removal of fluids
* Sterile suctioning if necessary
* Frequent oral hygiene
* Indications for suctioning: noisy respirations, restlessness, increased HR, Increased RR, mucus in airway
139
VAP “Ventilator Bundle”
* HOB@ 30 degrees
* Oral Care, brushing teeth and
chlorhexidine rinses
* Ulcer prophylaxis
* Preventing aspiration
* Pulmonary hygiene
* Sedation vacation
140
Extubation
Hyperoxygenate patient
*Thoroughly suction ET and oral cavity
*Rapidly deflate ET cuff
*Remove tube at peak inspiration
*Instruct patient to cough
*Monitor patient every 5 minutes; assess
ventilatory pattern for respiratory distress
141
PH range
7.35-7.45
142
PACO2 range
35-45
143
BICARB range
24-28
