Play a major role in the gas-blood barrier and gas exchange
Thin and susceptible to injury
Inflamed when exposed to inhaled toxins
Type 2 Alveolar Cells:
Produce, store, and secrete pulmonary surfactant
After injury, type 2 cells rapidly divide to line the surface and later differentiate into type 1 cells
AlveolarCapillaryMembrane (ACM):
Vessels of the ACM form a network around each alveolus
Large enough so each red blood cell membrane touches the capillary wall, allowing for efficient gas exchange
Hemoglobin is brought from its normal venous blood saturation level of 75% to its arterial saturation of more than 96%
Ventilation: movement of air into lungs (inhalation) and out of the lungs (exhalation.)
Ventilation perfusion relationships: “V/Q”, should be equally matched at ACM level for optimal gas exchange. Not the case, so normal v/q ratio is 4:5 or 0.8
three main causes of hypoxemia: alveolar hypoventilation, ventilation - perfusion mismatch, intrapulmonary shunting
Hypoxicvasoconstriction: typically blood vessels in the body dilate in response to hypoxia, the pulmonary vessels constrict when PaO2 is less than 60mmhg.
Occurs when portion of pulmonary capillaries perfuse un/under ventilated alveoli.
Thought to be a compensatory response to limit return of unoxygenated blood to the left side of the heart. If prolonged and generalized through the lungs, pulmonary hypertension results.
Lack of surfactant: Pulmonary surfactant functions to lower the surface tension of the alveoli -> stabilized the alveoli, increase lung compliance, eases the work of breathing. Disrupted -> lungs less compliant, work of breathing increases. Severe loss results in alveolar instability and collapse and impairment of gas exchange
Airleak disorders: conditions that result in extra alveolar air accumulation.
2 categories:
Pneumothorax: accumulation of air or other gas into the pleural space
Barotrauma/volutrauma: result of excessive pressure in the alveoli that can lead to extreme alveolar wall stress and damage to the ACM, causing air to escape into the surrounding spaces
Pulmonary embolus: a clot lodges in the pulmonary artery system, disrupting the blood flow to a region of the lungs, a massive PE occurs with the blockage of a lobar or larger artery, resulting in occlusion of the pulmonary vascular bed.
Pulmonary consequences: increased alveolar dead space, bronchoconstriction, compensatory shunting
Hemodynamic consequences: increase in pulmonary resistance and right ventricular workload
Oxygen Therapy: Methods of delivery include low-flow systems and high-flow systems
Low-flow systems provide supplemental oxygen directly into the patient’s airway at a flow of 8 L/min or less
Reservoir systems incorporate a device to collect and store oxygen between breaths
High-flow systems deliver oxygen in an amount sufficient to meet all inspiratory volume requirements
Oxygen Therapy Goal:
Ensure adequate cellular oxygenation
Oxygen is considered a medication and requires a physician’s order
Indication: Hypoxemia
Dose-response method: Administer the lowest possible level of oxygen that will achieve a satisfactory PaO2 or SaO2
Oxygen Therapy Complications:
Oxygen toxicity
Carbon dioxide retention
Absorption atelectasis
Nursing management includes confirming the device is properly positioned, replacing it if dislodged, and monitoring oxygen saturation with a pulse oximeter
Artificial Airways:
Types include pharyngeal airways, oropharyngeal airways, and nasopharyngeal airways
Endotracheal tubes (ETT) are used for short-term airway management
Rapid Sequence Intubation (RSI) involves several steps for intubation and post-intubation management
Artificial Airways:
Tracheostomy tubes are used for long-term intubation
Indications include avoiding complications from oral, nasal, pharyngeal, and laryngeal intubation
Complications of tracheostomy tubes include displacement, bleeding, infection, and more
Artificial Airways Nursing Management:
Involves humidification, cuff management, suctioning, and communication
Closed tracheal suction systems (CTSS) are used for suctioning
Passy-Muir® valve aids in communication
Invasive Mechanical Ventilation:
Indications, types of ventilators, ventilator mechanics, modes of ventilation, and complications are important aspects
Ventilator-induced lung injury, barotrauma, volutrauma, and other complications can occur
Invasive Mechanical Ventilation Weaning:
Factors for weaning, weaning methods, and nursing management during weaning are crucial
Synchronized intermittent mandatory ventilation (SIMV) trials and pressure support ventilation (PSV) trials are common methods
Results from extrapulmonary disorders + type 2 --> not enough oxygen is being brought into the alveoli… not enough ventilation
Alveoli are normal, just not enough for gas exchange
TX: can give O2 (doesn’t correct low ventilation), control pain, demonstrate deep breathing, IS
Ventilation/Perfusion mismatch
Most common cause is partially collapsed alveoli/atelectasis or partially filled alveoli or pulmonary edema (type 1)
Ventilation and blood flow are mismatched in various regions of the lung… blood flow goes by under ventilated alveoli or no blood to alveoli to pick up oxygen
Tx: supplementalO2
Intrapulmonaryshunting
Blood goes to arterial system without ventilation because most of the alveoli are filled with fluid or collapsed. (type 1)
Tx: need PEEP, BiPAP is no acidosis, minimal O2
ALF ABGs:
PaO2 less than 60
PaCO2 greater than 45
pH < 7.35
ALF Ventilation: maintain pH level
no acidosis: bipap or no bipap = bipap
if acidotic/ pH < 7.25: NIV or intubate = intubate
ALF nur interventions- positioning
good lung down
or HOB up
ALF nur interventions- prevent desat
perform procedures as needed
hyper oxygenate before suction
rest and recovery time
minimize oxygen consumption (limit activity, sedation, control fever)
monitor with pulse oximeter
ARDS diagnosis according to the Berlin Definition:
Timing: within 1 week of known clinical insult or new or worsening respiratory symptoms
Chest imaging: bilateral opacities (fluids) not fully explained by effusions, lobar/lung collapse, or nodules
Origin of edema: respiratory failure not fully explained by heart failure or fluid overload
Classification of ARDS dependent on oxygen levels:
Mild: PaO2/FiO2 ratio of 200-300, PEEP 5 or more
Moderate: PaO2/FiO2 ratio of 100-200, PEEP of 5 or more
Severe: PaO2/FiO2 ratio < 100, PEEP of 5 or more
ABG findings in ARDS:
Low PaO2 despite supplemental O2 leads to refractoryhypoxemia
PaCO2 initially low from hyperventilation (alkalosis) but eventually increases as the patient fatigues (hypoventilation/acidosis)
ALF nur interventions - secretion control
hydration
humidify oxygen
cough and suction
incentive spirometry
ARDS:
Direct injury: aspiration, near-drowning, pulmonary contusion, pneumonia, covid