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PaCO2 vs. HCO3
PaCO2
ACIDIC!! (when it increases, there is ACIDOSIS)
controlled by the lungs
can change within MINUTES
HCO3
ALKALOTIC (when it increases, there is ALKALOSIS)
controlled by the kidneys
changes overs HOURS to DAYS
anion gap - what is it? normal range?
the difference between positive and negative anions
in most instances of METABOLIC ACIDOSIS, there is an increase in the anion gap
normal range - 5-15 mEq/L
anion gap - why is it important?
it’s helpful in determining the cause of and/or response to treatment for metabolic acidosis
ex: if a patient with DKA presents with an anion gap of 25, one would expect the anion gap to decrease gradually as the patient responds positively to treatment (AND since electrolytes are assessed frequently, acidosis can be monitored through the anion gap without getting frequent ABGs)
problems associated with an INCREASE in the anion gap (hint: KUSSMAUL)
K - ketoacidosis
U - uremia
S - salicylate intoxication
M - methanol toxicity
A - alcoholic ketosis
U - unmeasured osmoles: ethylene glycol, paraldehyde
L - lactic acidosis: shock, hypoxemia
Acute Respiratory Failure - what is it?
a rapidly occurring inability of the lungs to maintain adequate oxygenation of the blood with OR without impairment of CO2 elimination
ABG would show PaO2 of 60 or less with OR without an elevation of PaCO2 to 50 or more with pH less than 7.30
Acute Respiratory Failure - Hypoxemic (conditions that lead to this type)
CONDITIONS causing LOW blood oxygen levels
ARDS
asthma
atelectasis
interstitial fibrosis
pneumonia
pulmonary edema (HF)
pulmonary embolism (MASSIVE)
smoke inhalation
Acute Respiratory Failure - Hypercapnic (conditions that lead to this type)
CONDITIONS causing HIGH blood PaCO2 levels
CNS depression from oversedation
COPD (acute exacerbation)
head trauma
musculoskeletal disorders or trauma
sleep apnea
status asthmaticus
Acute Respiratory Failure - Type 3 Hypoxemic AND Hypercapnic (conditions that lead to this type)
ARDS (late)
COPD (late, acute exacerbation)
status asthmaticus (late)
Acute Respiratory Failure - Hypoxemic (s/s)
pulmonary - tachypnea, adventitious breath sounds, accessory muscle use
cardiac - tachyarrhythmias (initial), bradyarrhythmias (late), HTN or hypotension, cyanosis (central (lips, earlobes))
neurological - anxiety, agitation
Acute Respiratory Failure - Hypercapnic (s/s)
pulmonary - shallow breathing, bradypnea, lungs may be clear or there may be adventitious breath sounds
neurological - progressive decreased level of consciousness (lethargic, obtunded, stuporous, unresponsive)
Acute Respiratory Failure - treatments
maintain airway/improve ventilation
positioning upright, suctioning, bronchodilator for wheezing, noninvasive ventilation, intubation if needed, repeat ABGs as needed
optimize oxygenation
adjust FiO2 to keep SaO2 about greater than 90; decrease FiO2 to 0.50 or less as soon as possible; do NOT allow hypoxemia to occur to “prevent O2 toxicity”; use PEEP/CPAP as needed; use pulse oximetry to monitor response to therapy
optimize circulation, cardiac output
manage hypotension, address cardiac arrhythmias
identify etiology; provide emotional support
Noninvasive Ventilation of ARF (CPAP - what is it?)
continuous positive airway pressure
indicated for patients with hypoxemic respiratory failure who have increased work of breathing (such as cardiogenic pulmonary edema)
settings include FiO2 and 1 pressure setting in cm H2O pressure
Noninvasive Ventilation of ARF (BiPAP - what is it?)
Bilevel positive airway pressure
indicated for patients with hypoxemic and/or hypercapnic respiratory failure
settings include FiO2 and 2 pressure settings (inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP)
IPAP assists ventilation and EPAP assists with oxygenation
Noninvasive Ventilation of ARF - ADVANTAGES
buys time for medical treatment to take effect
reduces WOB
decreases preload/afterload (due to increased intrathoracic pressure drawing blood in and pushing it out easier)
improves oxygenation
improves ventilation (BiPAP)
reduces atelectasis
prevents intubation and resultant risks
Noninvasive Ventilation of ARF - CONTRAINDICATIONS
hemodynamic stability or life-threatening arrhythmias
copious secretions
high risk of aspiration
impaired mental status/inability to cooperate (unable to protect airway)
suspected pneumothorax
life-threatening refractory hypoxemia (PaO2 less than 60 with FiO2 at 100%
high flow nasal cannula - how much oxygen can it deliver?
100% FiO2 and up to 60L/min
high flow nasal cannula - ADVANTAGES
able to provide high FiO2
heated and humidified oxygen may imporove secretion clearance and decrease aiway inflammation
able to meet high inspiratory flow demands of tachypniec patients
seems to promote alveolar recruitment and increase FRC (functional residual capacity - the amount of air left in the lungs AFTER a normal exhalation)
decreases dead space ventilation
more comfortable than CPAP or BiPAP masks, allows access to the mouth without removal of a mask
high flow nasal cannula - DISADVANTAGES
unable to deliver higher airway pressures (PEEP or CPAP), and the low levels of airway pressure provided are variable when mouth breathing
provides limited pressure support for a patient with hypercapnic respiratory failure
high flow nasal cannula - INDICATIONS
community acquired pneumonia (CAP)
cardiogenic pulmonary edema when NIV is not tolerated
preoxygenation prior to intubation
post-extubation (even in low-risk patients)
for a patient who refuses intubation (DNI) but accepts alternative treatment measures
COPD acute exacerbation - 3 types
emphysema
asthma
chronic bronchitis
COPD acute exacerbation - easier to inspire or expire?
easier to INSPIRE than EXPIRE (air gets trapped in the lungs)
COPD acute exacerbation - physiological consequences
dynamic hyperinflation occurs due to too much air in the lungs
air trapping and auto-PEEP
LOW expiratory flow rates
acute exacerbation results in V/Q mismatch due to a problem with ventilation and an increase in PaCO2
patient may have chronic CO2 retention; if so, the patient will have patial OR complete compensation and high HCO3 on ABG
can result in RV enlargement (cor pulmonale) and elevated CVP
COPD acute exacerbation - signs and symptoms
worsening dyspnea
increase in sputum purulence
increase in sputum volume
hypercapnia, hypoxemia
COPD acute exacerbation - MANAGEMENT
titrate FiO2 to PaO2 GREATER than 60 or SaO2 GREATER than 90% with care NOT to overcorrect hypoxemia and decrease respiratory drive (must address SEVERE hypoxemia; do NOT withhold oxygen only because hypoventilation may occur, cells still need oxygen!!!)
bronchodilator therapy (inhaled short-acting beta-agonist (SABA) such as albuterol; inhaled anticholinergics such as Ipratropium)
monitor LOC for decreased responsiveness
corticosteroid therapy (prednisone, methylprednisolone, fluticasone, budesonide, etc)
antibiotic therapy (when PNA is the trigger, such as piperacillin-tazobactam, amoxicillin, levofloxacin, etc)
proceed with mechanical ventilatory support if needed (invasive or non-invasive)