Respiratory Failure Flashcards
(97 cards)
1
Q
What is an ABG? What does it measure
A
Identifies respiratory and metabolic condition and measures how they are progressing with their diseas-state
PaO2
SaO2 (arterial oxygen saturation)
PaCO2 (PCO2)
pH
Bicarbonate (main buffering system)
2
Q
what does little a demonstrate
A
arteriolar pressure
3
Q
Who draws ABG? And where is it stuck?
A
Typically respiratory therapist inpatient
Put on ice and then done w/in 15 minutes
4
Q
What do you need to check and why before ABG?
A
Modified allen test
Check patency of ulnar side to make sure there
5
Q
Where is the majority of O2 seen?
A
Arterial oxygen saturation
Most of O2 that diffuses from the alveolus to the pulmonary capillary binds to hemoglobin
SaO2 is the proportion of RBCs with hemoglobin bound to O2
Most commonly measured by pulse oximetry
Level below 95% considered abnormal but needs to be below 89% to qualify for home O2 per Medicare guidelines
6
Q
What is the marker of oxygenation in a patient?
A
PaO2, only makes up 2% of the oxygen
But it is NOT picked up by hemoglobin
7
Q
What is an abnormal PaO2?
A
Considered abnormal if less then 80mmHg but needs to be 55mmHg or less to qualify for home oxygen per Medicare guidelines
8
Q
What is the best marker of ventilation?
A
PaCO2
basically indicates the amount of hydrogen ions
9
Q
What is a normal PaCO2
A
Considered abnormal if above 45mmHg or below 35mmHg
10
Q
How do you blow off CO2?
A
Carbon dioxide is an acidic gas so rapid or deep inspiration can “blow off CO2” and cause rapid respiratory alkalosis
11
Q
What is the most important buffer in the body and what regulates it?
A
Bicarbonate
Generated and excreted by the kidneys
12
Q
What is a slower response to abnormal pH?
A
The kidneys regulating bicarb
13
Q
What pH of the blood is healthy?
A
7.4
> 7.45 alkelemia
<7.35 acidemia
14
Q
What is the carbonic acid/bicarbonate buffering system equation?
A
Left side respiratory
Right side renal
CO2 + H20 –> H2CO3 –> HCO3 + H+
15
Q
What is pH determined by
A
the ratio of HCO3/PaCO2
bicarb/H+
16
Q
When compensating for an acid-base balance, what is important to keep in mind?
A
Compensation does NOT overshoot
17
Q
How to calculate an A-a gradient?
A
Difference between A (alveoli)-a
18
Q
How is a normal A-a gap calculated based on age?
A
(Age+10)/4
19
Q
What does an A-a gradient tell us if normal or elevated?
A
How it helps determine cause of hypoxemia
If normal
Hypoventilation
Low inspired O2
If elevated
V/Q mismatch
Shunt
Impaired diffusion
20
Q
What are the steps to interpreting an ABG?
A
- pH (pH < 7.35 is acidemia, pH > 7.45 is alkalemia) primary disorder
- Look at PaCO2 and see if it is respiratory (Respiratory acidosis – PaCO2 >45 Respiratory alkalosis – PaCO2 <35)
- Look at Bicarb level (An HCO3 level below 22 indicates metabolic acidosis, An HCO3 above 26 indicates metabolic alkalosis)
21
Q
What is the goal of compensation?
A
Get to normal range, but often does not happen
Complete or incomplete based on whether or not it gets back to normal range
22
Q
What are ideal pH, PaCO2, HCO3?
A
pH = 7.4
PaCO2 = 40
HCO3 = 24
23
Q
What is this? pH = 7.32
PaCO2 = 52
HCO3 = 19
A
Mixed acidosis (combined metabolic and respiratory acidosis)
24
Q
What is this?
pH = 7.34
PaCO2 = 50
HCO3 = 31
A
Respiratory acidosis with incomplete metabolic compensation
might have COPD with pneumonia, with acute
25
What is this?
pH = 7.38
PaCO2 = 24
HCO3 = 19
Metabolic acidosis with complete respiratory compensation
26
What is this?
pH = 7.46
PaCO2 = 42
HCO3 = 31
Metabolic alkalosis with no compensation
27
What is this?
pH = 7.39
PaCO2 = 41
HCO3 = 25
Normal
28
What is this?
pH = 7.42
PaCO2 = 51
HCO3 = 33
Metabolic alkalosis with complete respiratory compensation
Body does not overcompensate, so the cause will be in the same direction as the pH
29
What is the cause of respiratory acidosis?
Airway obstruction
Lung disease
Chest wall disease (elderly patient with kyphoscolisos - huntchback, causes compression)
Neuromuscular disease
Primary brain injury (ex. CVA, trauma), sleep apnea, drugs causing sedation like opioids.
hypoventilation and not blowing off the CO2
30
What are the causes of respiratory alkalosis?
Voluntary hyperventilation
Involuntary hyperventilation (anxiety states, asthma exacerbation, CNS disease)
Lung disease causing hyperventilation (remember back to PE lecture)
31
What are the causes of metabolic acidosis?
Either losing bicarb
Increased acid load
Impaired acid excretion
32
How do you reduce dx for metabolic acidosis?
Calculate the anion gap
33
What is the anion gap and how do you get these values?
Get a BMP or CMP to see if there is extra anions in the blood
Based on Na + K - Cl + HCO3
if it is greater than 12, then it is secondary acidosis
34
What are the differentials of anion gap acidosis?
MUD PILES
M – Methanol (ex. Windshield washer fluid, bad moonshine)
U – Uremia (BUN >60)
D – Diabetic ketoacidosis
P – Paracetamol (acetaminophen)
I – Isoniazid (TB), iron
L – Lactic acidosis
E – Ethylene glycol (ex. Antifreeze)
S – Salicylates (ASA)
35
If there is non-anion gap acidosis, what are the dx?
Diarrhea
Renal tubular acidosis
Caused by loss of bicarbonate or decreased acid (H+) excretion
36
What are the causes of metabolic alkalosis?
Too much ingestion or dehdration
Loss of H+ through vomiting
Hypokalemia
37
What is acute lung injury?
A term that encompasses a continuum of clinical and radiographic changes that affect the lungs causing respiratory failure in the critically ill patient
Characterized by acute severe hypoxia that is not due to the heart (non cardiogenic pulmonary edema)
Acute respiratory distress syndrome (ARDS) is the most severe form of this disease
something causes respiratory failure in a patient
38
What is the main disease state in COVID patients?
ARDS
39
What is ARDS?
It is most common form of non cardiogenic pulmonary edema and most severe form of acute lung injury
Causes hypoxemic respiratory failure
It’s estimated about 190,000 cases in the US each year
40
What MC causes ARDS?
Sepsis
41
Other than sepsis, what are some causes of ARDS?
Shock
Large aspiration pneumonia
Drugs and/or drug overdose
- Opioids, ASA, Amiodarone, Nitrofurantoin,Tricyclic antidepressants
Lung contusion (motor accident)
Toxic inhalation
Multiple transfusions (d/t autoantibody)
Near-drowning (after hours or days)
42
What causes ARDS?
Cytokine storm!
Pro-inflammatory cytokines are pivotal in causing lung injury
Damage occurs mainly at the capillary and alveolar cells
Pathological hallmark is diffuse alveolar damage
43
What happens to the damaged alveoli in ARDS?
This alveoli damage causes excess fluid in interstitium and alveoli itself
impaired gas exchange
decreased cmpliance (harder to move alveoli)
Increased pulmonary arterial pressure
Decreased surfactant
44
What is the diagnostic criteria
Acute onset within 1 week of known clinical insult (usually sooner)
Bilateral pulmonary infiltrates
Respiratory failure not fully explained by heart failure or volume overload
PaO2/FIO2 ratio < 300mmHg
45
What is FIO2 and what is it seen in ARDS?
FIO2 = 21%
Higher in ARDS patients because you need more o2 to saturate properly
46
What are the s/s of ARDS?
Rapid onset of profound dyspnea usually within 12-48 hours after the initiating event
SOB, tachypnea, intercostal retractions and crackles on physical exam
Marked hypoxemia occurs that does not respond to standard supplemental O2
Many patients with ARDS demonstrate multiple organ failure, particularly the kidneys, liver, cardiovascular system, CNS
47
What do you see in imaging of CXR?
diffuse or patchy bilateral infiltrates that rapidly progress and characteristically spare the costophrenic angles
normal heart size
air bronchograms in 80% (not diagnostic though) really dense fluid and dilation because of it
48
What do you need to r/o for ARDS?
cardiogenic pulmonary edema
pneumonia
49
How do you prevent ARDS?
Nothing is effective :(
50
How do you treat ARDS?
Treat the underlying condition that led to ARDS
Treat secondary conditions (sepsis)
Supportive care to help prevent complications (pain management, sedation, to lower O2 requirements)
Tracheal intubation mechanical ventilation, supplement O2 to maintain PaO2 above 55mmHg but keep FIO2 less than 60%
51
What is O2 toxicity?
Increases odds of seizures, retinal detachment
52
What is PEEP and what does it do? What are some complications?
Keeps positive alveolar pressure to keep from collapse
The lowest levels of PEEP that is effective.
Auto-PEEP can develop which can decrease venous return, reduce cardiac output and potentially cause hypotension
Also places patient at risk for barotrauma (ex. pneumothorax)
Has been shown to improve hemodynamic outcomes but not shown to improve mortality
53
Why do you keep ARDS patients in prone?
Heavy lungs from cytokines, heart moves away from chest wall when lying down so that there is more room for the lungs.
54
What is the only thing that reduces mortality in ARDS patients? What is a problem about this though?
Low Tidal Volume Ventilation (LTVV)
this prevents overexpansion of alveoli to reduce inflammation
Causes hypercapnia in order to oxygenate patients in the long wrong
55
What is the mortality with ARDS? ARDS w/ sepsis? What happens chronically?
Mortality ranges 30-40% and increases to 90% when associated with sepsis
Median survival is 2 weeks
Most survivors are left with chronic pulmonary symptoms that may improve with time (cough, dyspnea, lung fibrosis)
56
What is respiratory failure?
Inability of lungs to meet metabolic demands of the body?
57
How does phrenic nerve damage cause respiratory failure?
Loss of function of diaphragm
58
What are the two types of respiratory failure?
Type 1 – lungs fail to provide adequate oxygenation of the blood (PaO2 <60mmHg) - ventialation is fine (PCO2)
Type 2 - hypoxemic with issue of ventilation (low PO2 and elevatedPCO2) hypercapnic
59
What are some causes of type 1 hypoxemic respiratory failure?
Decreased inspired O2 tension (↓PIO2)
V/Q mismatch (COPD)
Diffusion limitation (fibrosis)
Intrapulmonary shunt
Pneumonia
Atelectasis
CHF
ARDS
Caused by disorder of heart, lungs or blood
Etiology can be evaluated by CXR
Normal CXR consider:
COPD
Intracardiac shunt (right to left)
Pulmonary embolism
o2 is not going to where it needs to go
60
What are the causes of hypercapnic respiratory failure (type 2)
Respiratory center dysfunction (medulla)
Drug overdose, CVA, tumor
Central Hypoventilation (congenital disorder - brain tells body not to breathe)
Neuromuscular disease
Polio, Myasthenia Gravis, spinal injuries, Guillain-Barre
Chest wall/Pleural diseases
Kyphoscoliosis, pneumothorax, large pleural effusion
Upper airway obstruction
Tumor, foreign body, laryngeal edema
Peripheral airway disorder
COPD, pulmonary fibrosis
Arterial pH is low
Causes:
Sedative drug over dose
Acute muscle weakness, ex. Myasthenia Gravis
Severe lung disease
Acute on chronic respiratory failure
Occurs in patients with chronic CO2 retention who acutely worsen and have rising CO2 and low pH
Caused by respiratory muscle fatigue in some cases
61
What are the s/s of hypoxemia?
Dyspnea (SOB)
cyanosis
restlessness, confusion, anxiety, tremor
62
What are the s/s of hypercapnia?
Dyspnea and headache are common
Signs:
Peripheral and conjunctival hyperemia
Tachycardia, tachypnea, hypertension
Impaired consciousness, papilledema, asterixis (dorsoflexion of hand causes rhytm pulsation)
63
What is the treatment of respiratory failure?
1) Specific therapy directed toward the underlying disease
Example: antibiotics for pna, anticoagulants for PE, bronchodilator therapy and corticosteroids for COPD exacerbation
Respiratory supportive care to maintain adequate gas exchange
General supportive care
64
What is the goal O2 sat in respiratory patients?
O2 sat at 90%, don't want to over oxygenate
65
What are the different forms of oxygen delivery
Nasal cannula
Nasal catheter
Simple mask
Partial rebreather mask
Non rebreather mask
Venturi mask
Oxygen tent
*For every liter increase in O2, FiO2 increases about 4%
trying to limit ambient room air the lower you go down the list, because when you breathe through your nose is also ambient air.
66
What is nasal cannula?
Common and inexpensive
Does not interfere with eating or talking, well tolerated
Higher flow rates can dry out the nasal mucosa fast (can add humidity)
Dependent on how much patient inhales through the nose
Low flow: 1-6 L/min (FiO2 of 24% to 44%) remember, each liter = 3-4%
High flow: up to 10 L/min
67
What is a nasal catheter?
Not used often since so uncomfortable
Inserted through the nostril with the end of the catheter resting in the oropharynx.
Needs changed to other nostril every 8 hours
68
What is a simple face mask? How long should it be used?
Has vents on both sides to allow room air to enter and exhaled CO2 to escape
Used when increased O2 delivery is needed for short periods (less than 12 hours)
Delivers FIO2 of 40 to 60% at flow rates of 5 L/min to 8 L/min respectively
Never use less then 5 L/min as patient may rebreathe most of their own air and become hypoxemic/hypercapnic
69
What is a partial rebreather?
Has a resevoir bag
most of airways is typically deadspace,
recycles the oxygen that has not diffused into the tissues
Delivers FiO2 of 35% to 60% at a flow rate of 6 L/min to 10 L/min respectively
O2 reservoir bag allows the patient to rebreathe the first 1/3 of exhaled air (dead space air)
It increases FIO2 by recycling expired O2
70
What is a non-rebreather mask?
Delivers the highest FiO2 possible 95% at a flow rate of 10-12 L/min
Two one-way valves prevent the following:
Entrance of room air during inspiration
Retention of exhaled gases during expiration
typically used in acute emergency and will eventually be on a ventilator
71
What is the venturi mask?
Delivers FiO2 varying from 24% up to 60% at flow rates of 4 L/min to 10 L/min
By mixing room air with precise amount of oxygen you can dial in the FiO2. The size of the port and oxygen flow rate determine the FiO2
often used in COPD patients where you do not want to over-oxygenate
72
What is a face tent?
Designed for patients who cannot wear a mask or nasal cannula (examples: facial surgery or trauma)
73
What oxygenation do you use in infants?
Oxygen hood
74
Pressure ventilation
Used in non-invasive ventilation where pressure is fixed but volume is variable
Like blowing into a balloon
75
What is a Noninvasive positive airway ventilation (NPPV) and what is it firts line for?
pressure ventilation
First line therapy in COPD patients with hypercapnic respiratory failure who can:
Protect their own airway
Handle their own secretions
Tolerate the BPAP mask
Reduces intubation rates and amount of ICU stay
76
What is Bilevel positive airway pressure (BPAP)?
Delivers preset inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP)
Most commonly used in patients with COPD, conditions causing respiratory muscle weakness and obesity hypoventilation
Patients must initiate each breath on most machines
important for type II with hypercapnia and hypoxemia (because they can blow off CO2)
77
What is CPAP?
Continous pressure
Continuous level of positive airway pressure throughout respiratory cycle
No additional pressure above the CPAP level is provided
Patients must initiate all breaths
Most commonly used in patients with sleep apnea or cardiogenic pulmonary edema
78
When do you intubate a patient?
Hypoxemia despite supplemental O2
Upper airway obstruction
Unable to protect airway or clear secretions
Acute hypercapnia that does not quickly respond to noninvasive ventilation (CPAP or BiPAP)
Progressive fatigue, mental status changes, tachypnea, or use of accessory muscles
Apneas
79
For intubation, what form is preferred?
Orotracheal intubation is preferred since easier, faster and less traumatic than nasotracheal
80
How should the tube be placed in intubation?
Position of the tip of the endotracheal tube should be positioned at the level of the aortic arch and verified by CXR
so that both lungs get O2, not just one
81
What happens if you overinflate a tube?
Cuff pressure should not exceed 20mmHg to minimize tracheal injury
82
What is mechanical ventilation?
Volume ventilation
Can fully or partially replace spontaneous breathing
Used for acute or chronic respiratory failure when there is insufficient oxygenation or ventilation, or both
Benefits include:
Improved gas exchange
Decreased work of breathing
More precise titration of oxygen needs
set the FIO2 precisely based on minute venitilation
83
What are the types of breaths?
Ventilator initiated: setting a respiratory rate and tidal volume and gives a breath
Patient-initiated breaths- patient effort causes flow change which initiates the breath
84
What is minute ventilation calculated?
MV = RR x Vt (tidal volume)
85
What are volume assist breaths
Breaths are initiated by the patient with a set inspiratory flow rate
Inspiration is stopped when the set tidal volume was delivered
86
What are volume controlled breaths?
Breaths are ventilator-initiated with a set inspiratory flow rate
Inspiration is terminated once the set tidal volume was reached
87
What is continous mandatory ventilation CMV Mode?
Most controlled form of ventilation
Minute ventilation is determined entirely by the set respiratory rate and tidal volume
Patient does not initiate additional breaths and does not require any patient effort
Patient may be on heavy sedation, pharmacologic paralysis, or in a coma
88
What is intermittent mandatory ventilation IMV Mode?
Set minute ventilation, but patient can increase the MV based on spontaneous breaths
89
What is Synchronized IMV (SIMV) Mode
Variation of IMV
Ventilator breaths are synchronized with patient effort
Support can range from full support to no support at all
Better patient-ventilatory synchrony, preserves respiratory muscle function, greater control over level of support
90
What is pressure support ventilation dependent on?
Effort of the patient
91
What is Pressure support ventilation (PSV) mode
Patient must trigger each breath, no set respiratory rate
The work of breathing is inversely proportional to the pressure support level
Useful when weaning a patient from mechanical ventilation
More comfortable mode
Patient has greater control
92
What is Positive end-expiratory pressure (PEEP) and some complications?
Generally added to ventilation to prevent alveolar collapse with end expiration
Usually around a pressure 5cmH20
With ARDS (using low tidal volume ventilation) up to 20cmH20 may be used
Potential complications:
Decreased cardiac output
Increased risk for barotrauma
Possibility of impairing cerebral blood flow (d/t decreased cerebral venous outflow which causes increased intracranial pressure)
Barotrauma (excessive tidal volumes, PEEP)
Pneumothorax
Subcutaneous emphysema (air escaping and can feel crepitus)
Pneumomediastinum
Ventilator-associated pneumonia (each day a patient is on a ventilator, risk of PNA increase by 1% because you are compromising oral pharynx)
Trauma - tracheal stenosis, vocal cord dysfunction
be mindful of giving too much pressure - risks are outweighed by the benefits
93
What is the mean survival rate of lung transplants?
6 years
94
What are the MC diseases that need lung transplant?
COPD
Idiopathic pulmonary fibrosis
Cystic fibrosis (typically duel because there is bilateral infection)
Alpha-1 antitrypsin deficiency
Idiopathic pulmonary hypertension
Coal Worker’s Pneumoconiosis
95
What determines whether or not you get a lung transplant?
Lung allocation score (LAS)
Want to wear out lungs - because you are trading one disease for another avg survival rate is 6 years
score based on how much the lungs will improve your life
96
What are the guidelines for lung transplant
Appropriate age (usually under age 65)
Severe lung disease that is progressive
Limited life expectancy because of their lung disease
Good nutritional status and BMI less than 30
Good support system and mentally intact
97
