Download 211 Gas Exchange Problems notes

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Neonatal intensive care unit wikipedia , lookup

List of medical mnemonics wikipedia , lookup

Transcript
1
Gas Exchange Problems
John Miller
Chronic Obstructive Pulmonary Disease (COPD)
●
●
Pathophysiology
●
●
Progressive, chronic airflow obstruction
Chronic bronchitis and/or emphysema
Characterized by slow progressive obstruction of airways
●
●
●
●
Resistance to airflow to increases.
Expiration becomes slow or difficult.
Mismatch between alveolar ventilation and perfusion
Impaired gas exchange
COPD Videos
Chronic bronchitis
●
●
●
●
Inhaled irritants cause chronic inflammation
Production of thick mucus
Narrowing of airways
Common recurrent infection
Pathophysiology of Bronchitis
 Inflammation of bronchi increases mucus
 Decreased ciliary function
 Decreased FEV1/FVC ratio
 The proportion of total volume of air that can be expired in the first second of expiration.
 The amount of air which can be forcibly exhaled from the lungs after taking the deepest breath
possible.
 Starts with large airways and spread to all airways.
 Reduces alveolar ventilation
 Abnormal ventilation-perfusion ratio develops and causes a lower PaO2.
 PCO2 increases
 Polycythemia develops
Emphysema
●
●
●
●
Destruction of the walls of the alveoli
Enlargement of abnormal air spaces
Airway collapse
Loss of alveolar surface area for gas exchange
Pathophysiology of Emphysema
 Alpha1 antitrypsin breakdown
 Alveolar wall destruction
 Partial airway collapse leading to obstruction, but not by mucous as in bronchitis
 Loss of elastic recoil
 Pockets of air in alveolar spaces (blebs) and lung parenchyma (bullae), can result in pneumothorax
 Results in increased dead space (areas not participating in gas or blood exchange)
 Destroys pulmonary capillaries
2
Manifestations
●
●
●
●
COPD is classified according to severity, staged from 0 to 4.
Productive cough, often in mornings
Dyspnea with activity, exercise intolerance
Presence of a barrel-shaped chest
Clinical Features and Manifestations of COPD
 Clinical Manifestations Generally for COPD
o All patients have some asthma, bronchitis, emphysema.
o Pulsus paradoxus
o Cor pulmonale, pitting edema, large liver, distended neck veins
o Prolonged expiration, exertional and rest dyspnea, pursed lip breathing, can only speak a few
words
o Flat diaphragm, bullae, raised shoulder girdle, cyanosis, larger back and neck muscles,
increased chest AP diameter
Pulsus paradoxus
 Inspiratory systolic BP lowered 10 mm or more, than expiratory systolic BP.
 Caused by negative pressures and increased pooling in lungs, which causes less blood to enter the
left ventricle and a subsequent decreased peripheral pulse.
Assessment When Bronchitis is Most Prominent
 40-50 years old
 Mucus, persistent cough
 Low PO2 (cyanosis), high PCO2
 Stocky build, cor pulmonale (right CHF, edema)
 High HCT
 Small airways first
Assessment When Emphysema is Most Prominent
50-75 years
 Cachectic, tachypnea
 Accessory muscles use
 PaO2 normal or slight decrease, no cyanosis usually
 Low or normal PCO2 until end stage
 Reduced FEV1
 No cor pulmonale until late stage
 Decreased breath sounds
Incidence and risk factors
●
●
●
●
●
●
Fourth leading cause of death in U.S
Cigarette smoking
Air pollution
Occupational exposures
Airway infection
Familial and genetic factors
Diagnosis
●
●
Pulmonary function tests
Ventilation–perfusion scanning
3
● Serum alpha1-antitrypsin levels
● ABGs
● Pulse oximetry
● Exhaled carbon dioxide
●CBC with WBC differential
●EKG
●Right ventricular hypertrophy
●Conduction pathway (axis) changes
●Chest x-ray
●Over inflated lungs
●Flattened diaphragm
●Large heart
Complications
●Pneumonia, which often leads to respiratory failure
●Spontaneous pneumothorax from a ruptured bleb
Medications
●
●
●
●
●
Immunizations against pneumococcal pneumonia and influenza
Broad-spectrum antibiotics for suspected infection
Bronchodilators
Corticosteroids when asthma is component
Alpha1-antitrypsin replacement therapy for those with genetic deficiency
Improve Ventilation: Bronchodilator
●Beta2 agonist (IV, oral, inhalation)


Albuterol, metaproterenol
Adverse effects: Tachycardia, tremor, nervousness, nausea
●Anticholinergic


Ipratropium (Atrovent)
Adverse effects: Dry mouth, nervousness, dizziness, fatigue, headache
●Methylxanthine


Theophylline
Adverse effects: GI upset, tachycardia, N&V, tremors, nervousness
●Corticosteroid


IV then oral on the third day, then tapered gradually.
Adverse effects: HTN, peptic ulcer, dysphoria, hyperglycemia, cough, thrush, fragile skin,
delayed wound healing, etc.
Treatments
●
●
●
●
●
Smoking cessation
Avoidance of airway irritants and allergens
Pulmonary hygiene measures
Adequate hydration
Pulmonary rehabilitation (PR)
4
●
Regular aerobic exercise, if applicable
Improve Ventilation
●Mechanical ventilation, become ventilator dependent
●Oxygen at 3 liters or less
●Keep pO2 at least 60 or a saturation of at least 90.
●Cannula or Venturi up to 32% FIO2 (fraction of inspired oxygen)
●Respiratory failure
●Highest flow (non-rebreather, reservoir mask) needed but may knock out respiratory drive so
that ventilation is also necessary.
●Position in high Fowlers.
●Caution with opioids, sedatives, tranquilizers
●Incentive spirometer, if ordered, 10 times per hour when awake
Control Complications
●Cor pulmonale is treated with diuretics and digoxin
●Polycythemia is treated with phlebotomy of 1 unit to reduce the HCT (if greater than 60) and
improve circulation
●Antibiotics to prevent pneumonia when sputum is colored
More Treatments
●
●
Oxygen
●
Long-term oxygen therapy
Surgery
●
●
●
Lung transplant
Lung reduction surgery (LVRS)
●Part of emphysematous lung is removed.
●Increases FEV1 and vital capacity (VC).
Bullectomy to prevent pneumothorax
Complementary therapies
●
●
●
Dietary measures
Herbal remedies
Acupuncture
Improve General Health
●Stop smoking
●Avoid high altitudes
●Supplemental oxygen:
–If on mask, switch to cannula for meals.
Improve Nutrition
●Eat enough calories, high protein
●Less carbohydrate, more fat, to reduce CO2 production.
●Small frequent meals
5
●Eat more earlier in day if tired later
●Schedule inhalers after meals so the food taste is not altered.
●Monitor nutrition with hemoglobin, albumin, and pre-albumin levels
●Adequate hydration
Remove Bronchial Secretions
●Nebulized bronchodilator
●CPAP, BIPAP, or PEEP with ventilation devices to keep airways open
●Postural drainage
●Chest physiotherapy
●Percussion (clapping on the chest) to loosen secretions
Promote Exercise
●Aerobic
o
o
Strengthens respiratory muscles
Walking
●Breathing
o
o
o
Diaphragmatic
Pursed lip
Avoid rapid shallow breathing
●Stop or slow activity where the respiratory rate, pulse, and mental status do not return to
baseline within three minutes.
●Oxygen with exercise to keep saturation adequate.
●Exercises after respiratory treatments.
Assessment
●Breath sounds and respirations
●Assess lung function every four hours or more often.
●Assess before and after coughing (including breathing treatments).
●Assess mucous membranes every two hours.
Avoid conditions that increase O2 demand.
●Smoking, temperature extremes, excess weight, stress
●Help the patient manage anxiety.
●Fan
●Quiet
●Open doors and curtains.
●Relaxation techniques
Energy Conservation
●Help patient use energy conservation techniques.
●Pace activities throughout the day, with rest periods.
●Alternate high and low energy tasks.
●Keep a diary of activities at home for the nurse to evaluate.
●Adequate sleep
6
o
o
No stimulants (other than bronchodilators)
High protein snack, warm beverage, etc.
Self Care
●Support groups
●Sexual activity
●Infection prevention
●Flu vaccination yearly, Pneumococcal vaccination every six years
●Avoid pulmonary irritants
●Perfumes, fragrances, wood or other smoke
●Smoking cessation
●Breathing improvement starts quickly.
●Use counseling and medications.
Nursing Care
●
●
Diagnoses, outcomes, and interventions
●
●
●
●
Ineffective Airway Clearance
Imbalanced Nutrition: Less Than Body Requirements
Compromised Family Coping
Decisional Conflict: Smoking
Continuity of care
●
●
Adequate fluid intake
Avoid respiratory irritants, prevent infection
Pulmonary Embolism
●
●
●
Also known as thromboembolism
Embolus obstructs blood flow in part of pulmonary vascular system
A medical emergency
●
Fifty percent of deaths occur within first 2 hours following embolization.
Pathophysiology
●
●
●
A match between blood flow through perfusion and lung ventilation is necessary for effective
respiration.
●Perfusion decreased
●Ventilation unaffected (VQ mismatch)
●Results in hypoxemia
Impact depends on size and nature of embolus, secondary effects of obstruction.
Large pulmonary artery occlusion
●
Can cause sudden death: reduces cardiac output causing shock and bronchial constriction
●Lung tissue infarction from occlusion of significant portion of smaller vessels
● Obstruction of small segment of pulmonary circulation
● Might cause no permanent injury
7
Etiology and risk factors
●Deep calf, femoral, popliteal, or iliac veins
●Other sources: tumors, air, fat, bone marrow, amniotic fluid, sepsis, heart valve vegetation in
endocarditis
●Major operations: hip, knee, abdominal, pelvic
●Myocardial infarction
●Obesity
●Inactivity
●Oral contraceptives
●Prophylaxis to reduce risk
Manifestations
●
●
●
●
Depend upon size and location
Small emboli can be asymptomatic.
Common manifestations
●
●
Dyspnea, pleuritic chest pain, anxiety, cough
Similar to myocardial infarction
Manifestations of fat emboli
●
●
Sudden onset of cardiopulmonary and neurologic symptoms
Petechiae on chest, arms
●Crackles, hemoptysis
Complications
●Shock
●Respiratory failure
●Dysrhythmias
Diagnosis
●
●
●
●
●
●
●
●
Plasma D-dimer levels
Chest CT with contrast
Lung scans: Ventilation Perfusion Scan (VQ)
Pulmonary angiography
Chest x-ray
Electrocardiogram
ABGs
●Low pO2, low pCO2, high pH-hyperventilation
●Late decompensation: respiratory acidosis
Coagulation studies
8
Medications
●Anticoagulant therapy
o
o
Heparin therapy
Warfarin sodium
●Thrombolytic therapy
●Inotropes: Digoxin
●Sodium Bicarbonate for acidosis
●Analgesics: Morphine
Heparin
●Prevent further clots or extension of existing clots.
●Heparin (unfractionated) IV bolus and continuous infusion
●Therapeutic activated partial thromboplastin time (aPTT) level is more than 60 seconds or 1.52.5 times the baseline.
●Anti Xa factor is more standardized measurement based on aPTT
●Nomogram orders
●Protamine antagonist, hold ASA and other anticoagulants
●Low molecular weight Heparin SC (LMWH)
●If hemodynamically stable (not in shock)
●Requires no blood testing.
Warfarin (Coumadin)
●Keep International Normalized Ratio (INR) at 2.5-3 (higher than DVT).
●The INR is based on the Prothrombin Time (PT) and is used to standardize the varying PT
results between different labs.Takes 2-3 days to replace heparin anticoagulation effect.
●Vitamin K in diet (found in green leafy vegetables which is antagonist).
●Do not increase or decrease the amounts.
●Hold other anticoagulants such as ASA.
●Check for other drug interactions.
Anticoagulant precautions
●Soft sponge tooth brushes
●At least 10 minute pressure on punctures
●Observe for
o
o
Bleeding
Flank pain
●Avoid or minimize trauma
o
o
o
o
Bruising
Injections
Increased fiber
Prevent falls
9
More Treatment
●Endovascular management
o
o
o
o
Inferior vena cava filter
Greenfield filter, umbrella like
Less effective than anticoagulation (use when contraindicated)
Inserted through iliac vein or neck vein
●Pulmonary embolectomy
o
Used with hemodynamically unstable clients or those with contraindications for
thrombolytics
●Fibrinolytic therapy
o
o
o
For hemodynamically unstable clients.
Lyse clots and restore right-sided heart function.
May still be a high mortality rate.
Nursing Care
●
●
Diagnoses, outcomes, and interventions
●
●
●
●
Impaired Gas Exchange
Decreased Cardiac Output
Ineffective Protection
Anxiety
Continuity of care
●
●
●
Use of prescribed medicine
Reduce risk of bleeding
Avoid aspirin
Acute Respiratory Failure
●
●
Consequence of severe respiratory dysfunction
Defined by arterial blood gas values
●
●
An arterial oxygen level of less than 50–60 mmHg
Arterial carbon dioxide level of greater than 50 mmHg
Respiratory Failure Types
●
●
●
Hypoxemic failure type
●
●
Causes
● Pulmonary edema, drowning, ARDS, pneumonia, bleeding
Low PO2. Respond little to increases of oxygen even with ventilation.
Ventilatory failure type
●
●
●
●
PaO2 of 50 or less
pH of less than 7.25
Chronic elevated PCO2, increase of 5 mm or more
Also have hypoxemia, with low PO2.
Minutes to hours to days progression
10
Ventilatory Failure: Etiology and Risk Factors
●
●
●
Acute ventilatory failure is the inability to sustain a respiratory drive or inability of the chest wall /
muscles to move air in and out.
Increased workload for ventilation
Decreased ability of lung to meet oxygen demand
Ventilatory Failure: Risk factors
●
●
●
●
●
●
CNS: increased intracranial pressure, drug overdose
PNS: multiple sclerosis, Guillain-Barre’, spinal cord injury, myasthenia gravis
Musculoskeletal and pleural: flail chest, pleural effusion, pneumo or hemothorax, morbid obesity
Conducting airways: trauma, bronchospasm, epiglottitis
Lungs: COPD, pulmonary emboli, pulmonary edema, ARDS
Nonpulmonary problems: sepsis, MI, anaphylaxis, shock, DIC
Pathophysiology
●
●
●
●
COPD is most common cause.
● Acute drop in blood oxygen levels
● Increased carbon dioxide levels
Failure of oxygenation
● Hypoxemia without a rise in carbon dioxide levels
Hypoventilation
● Hypoxemia with hypercapnia
Effects of shock on body systems
● Respiratory system
● Impaired oxygen delivery to cells
● Respiratory rate increases
● Decrease in perfused alveoli
● Gas exchange impaired
● Oxygen levels in blood decrease, carbon dioxide levels increase
● Respiratory acidosis
● Acute respiratory distress syndrome (ARDS)
More Pathophysiology
●
●
●
Failure of alveolar ventilation leads to a ventilation/perfusion (VQ) mismatch.
●
●
Increases PCO2 levels.
Respiratory acidosis develops.
Residual pressure (FRC or functional residual capacity) causes alveolar collapse.
●
●
Prevents oxygenation and blood flow to the alveoli.
Decreases lung compliance.
Shunt occurs with blood flow but no ventilation.
Causes of Respiratory Failure
Manifestations
●
●
●
Dyspnea
Restlessness, apprehension
Impaired judgment
11
●
●
●
●
●
Motor impairment
Tachycardia
Hypertension
Cyanosis
Dysrhythmias
The Patient with Acute Respiratory Failure
●
Manifestations and course
●
●
●
Hypotension
Decreased cardiac output
Prognosis varies
● Resolves quickly without long-term effects in uncomplicated drug overdose
● Course prolonged, outcome less favorable in underlying lung disease
Diagnosis and Medications
●
●
Diagnosis
●
●
Exhaled carbon dioxide
Arterial blood gases
Medications
●
●
●
●
●
Beta-adrenergics or anticholinergics
Methylxanthine bronchodilators
Corticosteroids
Antibiotics
Sedation and analgesia
Treatment
●
Oxygen therapy
●
●
Reverse hypoxemia
CPAP used if failure caused by hypoventilation
Airway management
●
●
●
●
●
●
●
●
●
●
●
Endotracheal tube cuffed with air-filled or foam sac
Nasal or oral
Loose objects such as dentures are removed.
Supine, with head hyperextended.
MD or nurse anesthetist uses a laryngoscope in oral method to visualize cords.
Should take about as long as can hold breath (30 seconds).
Position of ET tube is verified by stethoscope (equal breath sounds), pulse oximetry, end tidal CO2
monitor, chest X-ray.
Tube is secured with tape or holder and bite block.
Record where the tube meets the lips. Any movement can necessitate reintubation.
Nasal route used less because of sinusitis.
Tracheostomy for long term
12
ET Intubation
ET Tube Cuff
●
●
●
Part of ET tube, which separates upper trachea from lower trachea.
Inflation
●
●
Seals the tube to allow ventilation and to protect from gastric aspiration.
Keep pressure low enough to prevent ulceration and necrosis of trachea. Use minimal
occlusion volume technique: with stethoscope, inflate cuff to point where air leaking heard
stops.
Deflation
●
●
Only when moving tube or adjusting cuff volume.
Must suction before deflating, as oral secretions will drop down into trachea from above the
cuff.
●
Leaks
●
If tear or hole in cuff, will have to replace entire ET.
●
May need more air in cuff to seal.
Mechanical ventilation
●
Modes of ventilation
●
●
●
●
●
●
●
●
●
Noninvasive ventilation (NIV)
Continuous positive airway pressure (CPAP)
Assist-control mode ventilation (AC)
Synchronized intermittent mandatory ventilation (SIMV)
Positive end-expiratory pressure (PEEP)
Pressure support ventilation (PSV)
Pressure-control ventilation (PCV)
Independent lung ventilation
High-frequency ventilation
Ventilator Videos
Synchronized Intermittent Mandatory Ventilation (SIMV)
●
●
●
Machine requires some preset breaths at a certain volume. Machine breaths are
synchronized with spontaneous breaths.
Patient can breathe spontaneously on own also at own volume and rate.
Used in decreased lung compliance (elasticity) or increased airway resistance
(bronchospasm).
Pressure Control Mode of Ventilation
● Used to get the highest oxygen levels with the lowest FIO2s.
● Keeps alveoli open during expiration and reduces shunting.
● Types
● NPPV
●Continuous positive airway pressure (CPAP)
● Mechanical ventilation
13
● Positive end-expiratory pressure (PEEP)
● 10-25 cm of H2O pressure
●Complications: VQ mismatch, subcutaneous emphysema, decreased cardiac output
Ventilator settings
●
●
●
Rate
Tidal volume
Percentage of oxygen delivered
Complications
●
●
Nosocomial pneumonia
Barotrauma (volutrauma)
●
●
●
Subcutaneous emphysema
Pneumothorax
Pneumomediastinum
●
Cardiovascular effects
●
Gastrointestinal effects
●
●
Decrease in cardiac output
Stress ulcers leading to hemorrhage
Physiologic Changes After Mechanical Ventilation
●
●
●
●
●
●
Decreased cardiac output, low BP, shock
Alveolar stretch injury causes inflammation.
Ischemic gastric mucosa causes bleeding and ulceration.
Decreased spleen and kidney blood flow and increased ADH causes renal failure.
Cerebral edema in hyperventilation causing seizures and other neurological changes.
Oxygen toxicity if FIO2 of 0.7 or more for 24 hours, leading to lung stiffening (decreased
compliance).
Weaning from Ventilator
●
●
●
T-piece or CPAP
SIMV and PSV
Terminal weaning
●
●
●
When survival without assisted ventilation is not expected
Quiet medical–surgical or hospice room
Analgesia and sedation for comfort
Nutrition and Fluids
●
●
●
Mechanical ventilation promotes sodium and water retention.
Enteral or parenteral nutrition
Nasogastric, gastrostomy, or jejunostomy tube to reduce risk of regurgitation, aspiration
Nursing Care
●
Diagnoses, outcomes, and interventions
14
●
●
●
●
●
Impaired Spontaneous Ventilation
Ineffective Airway Clearance
Risk for Injury
Anxiety
Continuity of care
●
●
Prevention
Pulmonary hygiene measures
Nursing Management
●
Frequent assessment
●
Q1-2 hours and with any change.
● Vital signs
● CNS
● Breath sounds, respiratory character and rate, SpO2, ABGs
● Arrhythmias
● Check ET mark at lips.
Medications
●
●
●
●
Neuromuscular blocking agents if not breathing with the machine
Pancuronium, vercuronium
Combine with a sedative or anxiolytic drug
Pain medication may be necessary
EndoTracheal Suctioning
●
●
●
●
●
●
Perform only when secretions are present.
Sterile, hyperoxygenate before and after
Good technique helps prevent ventilator associated pneumonia, a nosicomial infection.
80-120 mm suction to prevent tissue trauma
Saline instilled in ET if secretions tenacious.
Closed suction better than open suction where ET is disconnected from ventilator.
Alarms
●
●
●
High pressure
●
●
●
●
●
Decreased compliance
Secretions
Biting on tube, coughing
Not breathing with the ventilator
Sedation after checking machine, suctioning.
Low pressure or low minute volume (TVxRR)
●
●
●
Disconnection
Cuff leak
Apnea
Never silence alarms
15
Other nursing care
●
●
●
●
●
●
●
Turn Q 2 hours.
Adequate humidity. Drain away from patient to prevent contamination.
Reduce anxiety and stimulation
Find best communication method since cannot talk with ET.
Watch for accidental extubation: throaty sounds, vent low pressure alarm. Ambu bag until
reintubation.
Oral care Q2 hrs. Swab, lubricate (no lemon or alcohol) mouth and lips, suction. Check for
pressure sores from tube. May have to be moved carefully to other side.
Nutrition with TPN or enteral feedings. Usually have NG tube. Keep head elevated to prevent
reflux and VAP.
Weaning and Extubation
●
Weaning from the ventilator
●
Extubation
●
●
●
●
●
Gradually lower settings, remove sedation.
After breathing on own with ET in, good ABGs, assessment
Hyperventilate, suction ET, hyperventilate, loosen tape, suction as tube removed, humidified
oxygen after, coach breathing
Ventilator dependent patients
COPD patients difficult to get off machine
Acute (Adult) Respiratory Distress Syndrome
●
●
Non-cardiac pulmonary edema and refractory hypoxemia
40% lead to mortality due to multiple organ system dysfunction
Pathophysiology
●
●
Acute lung injury
Unregulated systemic inflammatory response
●Release of vasoactive substances such as histamine and serotonin
● Reduction of gas exchange
● Fibrotic changes in lungs
● Tissue hypoxia
● Metabolic acidosis
●Increases alveolar membrane permeability.
●Fluid leaks into interstitial and alveolar areas.
●Causes pulmonary edema.
●Reduces lung compliance (elasticity).
●Impairs oxygen transport
VQ Mismatch
Conditions Associated with the Development of ARDS
Manifestations
●
Develops 24–48 hours after initial insult
16
● Dyspnea, tachypnea, anxiety
● Progressive respiratory distress
● Cyanosis does not improve with oxygen administration less than 40%
●PaO2 less than 60, pCO2 elevated
● Respiratory alkalosis first, then respiratory acidosis
Dyspnea, cough, thick frothy sputum (pulmonary edema-severe CHF)
Diagnosis
●
●
●
●
●
Refractory hypoxemia is the hallmark of ARDS.
ABGs
Chest x-ray
●Chest X-ray: diffuse, bilateral, and rapidly growing infiltrates
●White areas referred to as a snowstorm or whiteout.
Pulmonary function tests
Pulmonary artery pressure monitoring
Medications
● No definitive drug therapy
● Inhaled nitric oxide
● Surfactant
● NSAIDs
● Corticosteroids: Methylprednisolone
●Loop Diuretics: Furosemide
● Glycoside Inotropes: Digoxin to increase contractility
●Antibioticcs
Other Treatments
●
Mechanical ventilation
●Same as for ventilatory failure plus:
●PEEP
●Nitrous oxide to dilate the lung capillary bed, which reduces the pulmonary hypertension
●Antioxidants and prostaglandins
●Prone positioning, which changes the blood flow and damage pattern to the lungs. This may also
help in other ventilated patients.
●Kinetic therapy, where the patient is on a continuously rotating bed.
ventilated patients.
●
●
Extubation
Attention to nutrition, fluid replacement
Complications
●Same as those for Ventilatory failure plus:
●Lung fibrosis
●Thrombocytopenia
●Sepsis
These may be used on all
17
●Disseminated intravascular coagulation (DIC)
Nursing Care
●
●
Diagnoses, outcomes, and interventions
●
●
Decreased Cardiac Output
Dysfunctional Ventilatory Weaning Response
Continuity of care
●
●
●
Teach about causes
Avoid exposure to irritants
Obtain immunization
http://americannursetoday.com/top-10-care-essentials-for-ventilator-patients/