Acute Respiratory Failure Flashcards
acute resp failure
A condition in which the resp system fails in one or both of its major functions: gas exchange and ventilation
PCO2 <45, pH <7.35, PaO2 <60
how is ARF diagnosed?
ABGs, CXR, C&S (sputum/blood) and supported by physical assessment.
- clinical presentation
- history
- CBC
- CT scan (CNS causes, chest trauma)
- V/Q scan (PE)
T or F: ARF is the most common type of organ failure seen in critical care units with ~56% of patients in CC experiencing it.
True
____ of patients with ARF need mech vent and die in hospital from it
1/3
types of resp failure
type 1, type 2, mixed
type 1 resp failure
acute hypoxemic respiratory failure: the primary problem is a defect in gas exchange
type 2 resp failure
acute hypercapnic respiratory failure: the primary problem is inadequate ventilation
mixed resp failure
difficult to locate the primary source of the
respiratory failure…giving rise to patient
responses related to both impaired gas exchange and ventilation
management of ARF is broken down into 2 main categories which are ______
treatment of primary cause
supportive medical management
treatment examples
pneumonia - give abx
PE - give thrombolytics
anesthesia - provide reversal agent or let wear off
supportive management
- multipronged approach
- promoting adequate gas exchange (supplemental O2, PPV)
- correcting acidosis
- pharmacological intervention (bronchodilators, steroids, sedation, analgesia, paralytics)
- initiating nutritional support
- preventing further complications
non-invasive vs invasive ventilation
- non invasive = CPAP (oxygenation), BiPAP (ventilation and oxygenation)
- invasive ventilation = ETT, trach
bronchodilators
- beta agonists (salbutamol, ipratropium)
- goal is to decrease airway resistance and dilate airways
steroids
- oral (prednisone), inhalation (fluticasone), IV (hydrocortisone)
- dose and delivery are all dependent on pt condition and history
- used to reduce airway inflammation
sedation
- depends on pt situation
- used to assist with and maintain adequate ventilation, comfort patient, decrease WOB
how much sedation would you give if a pt is on non-invasive ventilation?
sedation up to the point of decreasing anxiety RASS of 0 or -1 is: ativan or small doses of midazolam
how much sedation would you give if a pt is on invasive ventilation?
- sedation to ensure that the individual is able to tolerate the breathing tube and mechanical ventilation. pt-dependent so may range from RASS of 0 to -5
- can be accomplished with benzodiazepines (midazolam infusion or bolus), alpha 2 agonist (precedex) or general anesthetic (propofol)
- always set pt specific goals
paralytics
- used rarely and only in specific situations
- if unable to ventilate patient
- intubation
- IF using paralytics ensure that the patient is adequately sedated prior to administration!!
correct acidosis: what does hypoxemia cause? impaired ventilation leads to ____? what should we correct?
- hypoxemia causes impaired tissue perfusion, production of lactic acid and development of metabolic acidosis
- impaired ventilation lead to CO2 accumulation and respiratory acidosis
- correct oxygenation and ventilation and acidosis should correct
should we use sodium bicarb in correcting acidosis?
NO - minimal benefit, can make worse; shifts the oxy-hemoglobin dissociation curve to left and can worsen tissue hypoxia
nutritional support
- essential part of healing
- ensure pt is receiving adequate calories in relation to metabolic demands
- commonly overlooked
- don’t overfeed - can increase CO2
- don’t underfeed - decreases ventilation drive and muscle strength
potential complications
- ischemic-anoxic brain injuries
- cardiac dysrhythmias
- venous thromboembolism
- stress ulcers
- GI bleed
- barotrauma, infection, injury from vent
- infection, injury, dislodgement from artificial airways, nutrition, arterial and venous cannulation sites
nursing management
- positioning (HOB elevated, good lung down, frequent repositioning)
- prevent desat (hyperoxygenate prior to suction, spacing out activities/care, ensure equip secure, administer pain/sedation PRN, control fever to control demand)
- promote secretion clearance (hydration, suction)
- pt and family teaching
pneumonia: what is it? who is most at risk?
- acute inflammation of the lung parenchyma caused by an infectious agent that can lead to alveolar consolidation
- most at risk are elderly, cardiorespiratory disease and/or immunosuppression
- symptoms can vary from mild to severe
- 8th leading cause of death overall
classification of pneumonia
- site of acquisition (most important for treating pathogens appropriately)
- causal agent
- severity
site of aquisition
CAP, HCAP, HAP, VAP
VAP
subset of HAP; development of pneumonia after artificial airway
gram positive
staph: presents in clusters
strep: present in chains
gram negative
- generally more damaging/toxic
- usually in rods
- e. coli, pseudomonas, enterobacter
VAP: what is early onset vs late onset and causes?
- early onset: 48-72 hrs after intubation
- often caused by staph aureus, strep pneumonia and H. influenzae
- late onset: > 72 hrs since intubation
- often caused by MRSA, pseudomonas and enterobacter
VAP signs and symptoms
need to consider if pt was intubated already for a reason
look for change in:
- CXR (consolidation? new infiltrates?)
- New or increasing Sputum/secretions (amount, colour, consistency)
- ABGs (worsening gas exchange or ventilation)
- Increasing or new fever (indicates a new infection or an infection not being treated for)
- New or increasing WBCs
- Cultures
common reasons for VAP
ETT bypasses many of the lungs normal defenses and creates a fast track for contamination
1) Aspiration of gastric contents
2) Bacteria from the stomach wicking up gastric tubes
3) Micro-aspiration of pooled secretions above cuff
patho of how VAP occurs
- Normal defense system of the body (cilia in nose and protective mucus) are circumvented, allowing mouth colonization with pathogenic bacteria.
- Decreased LOC (with sedation) makes patients more prone to aspiration
- Gastric colonization of pathogenic bacteria as a result of increased gastric alkalinity due to antacid or H2 blocker use
VAP main risk factor
ETT: direct passage into lungs; prevents cough. prevents upper airway filtering/humidification, inhibits ciliary transport by epithelium, direct conduit into lungs for airborne pathogens, reservoir for pathogens allowing biofilm to form, cuff provides place for secretions to pool in hypoglottic area
other risk factors for VAP
- Age > 65 years old
- Underlying chronic illness (e.g. COPD, emphysema, asthma)
- Immunosuppression
- Depressed consciousness
- Thoracic or abdominal surgery
- Previous antibiotic therapy
- Previous pneumonia or remote infection
- Nasogastric tube placement
- Gastric over distension
- Stress ulcer treatment
- Supine patient position
- Nasal intubation route
- Instillation of normal saline
- Nonconformance to hand washing protocol
- Indiscriminate use of antibiotics
- Lack of training in VAP prevention
how to prevent VAP
- strive for extubation
- work to minimize sedation
- re-evaluate RASS goals everyday
- mobilize
supportive management of VAP
- abx
- enteral feeding
benefits of adequate nutrition
- Reduces risk of nosocomial infection
- Improves wound healing
- Decreases mortality
- Prevents bacterial translocation
most common prokinetic/motility agents
maxeran
in rare and special cases, is erythromycin
if prokinetics don’t help, what should be done next?
small bowel feeding tube - goal is to bypass the issue of gastric emptying and feed directly into the duodenum
elevated blood sugar levels can…
- Impair immunologic response to infection
- GI motility
- Increase cardiovascular tone
goal blood sugar level range in ICU
6-10
