2 Exam- Banick

Front 1

Purpose/Indication
of mechanical ventilation

Back 1

Assist in elimination of CO2 when patient unable (treat hypercarbic respiratory failure)
Assist in uptake of adequate oxygen when patient unable (treat hypoxemic respiratory failure)
Treat both – which may co-exist!

Front 2

Hypoxia

Back 2

Sub-normal oxygen level

Front 3

Sub-normal oxygen level

Back 3

Hypoxia

Front 4

Hypoxemia

Back 4

An abnormally low amount of oxygen in the blood, the major consequence of respiratory failure. This results in low oxygen delivery to tissue.
Generally PaO2 < 60 mm Hg O2 saturation < 90%, but varies

Front 5

An abnormally low amount of oxygen in the blood, the major consequence of respiratory failure. This results in low oxygen delivery to tissue.
Generally PaO2 < 60 mm Hg O2 saturation < 90%, but varies

Back 5

Hypoxemia

Front 6

Hypercarbia

Back 6

Elevated CO2 levels in the blood (generally >45 mmHg)
Major effect is formation of carbonic acid = acidemia: {CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-}

Front 7

Elevated CO2 levels in the blood (generally >45 mmHg)
Major effect is formation of carbonic acid = acidemia: {CO2 + H20  H2CO3  H+ + HCO3-}

Back 7

Hypercarbia

Front 8

Hypoxemic Respiratory Failure 1
Classification of hypoxemia
Based on what relationship?

Back 8

DO2 = O2 content (CaO2) x Cardiac output (CO)
Where:
DO2 = Oxygen Delivery
CaO2 = (O2sat x HgB x 1.34) + (0.003) x PaO2

Front 9

Hypoxemic Respiratory Failure 2
Hypoxemia results from four disorders

Back 9

1. Insufficient O2 saturation
Lung problems (COPD, Pneumonia)
Shift of oxyhemoglobin-saturation curve
2. Insufficient HgB
Anemia
3. Malfunctioning HgB
Poisoning of metabolic pathways (CN, CO poisoning)
Change in hemoglobin affinity for oxygen
Acidemia, hyperthermia, hypercarbia = LESS (right shift)
Alkalemia, hypothermia, high altitudes = GREATER (left shift)
4. Insufficient circulation (CHF)

Front 10

what drives the O2 sat curve to the left?

Back 10

Higher Affinity:
Alkalemia
Hypothermia
Fetal HgB
Abn. HgB

Front 11

What drives the O2 saturation curve to the right?

Back 11

Lower Affinity:
Acidemia
Hyperthermia
Hypercarbia
2,3,DPG

Front 12

When can 2,3,DPG elevated?

Back 12

-excercise
-transfusion
-shock
-anemia
-acute coronary syndrome

Front 13

What effects CO2 and O2?

Back 13

The greatest determinant of CO2 elimination is minute ventilation (VE):

VE = Tidal volume (Vt) x Resp.rate (R)

The greatest determinants of O2:
The inspired fraction of oxygen (FIO2)
Best surrogate marker is the O2 saturation

Front 14

The greatest determinant of CO2 elimination is

Back 14

The greatest determinant of CO2 elimination is minute ventilation (VE):

VE = Tidal volume (Vt) x Resp.rate (R)

Front 15

The greatest determinants of O2:

Back 15

The greatest determinants of O2:
The inspired fraction of oxygen (FIO2)
Best surrogate marker is the O2 saturation

Front 16

Causes of Hypoxemia 1

Back 16

Inadequate transfer of O2 from environment to alveoli
Inadequate transfer of O2 from alveoli to circulation
Calculation of Alveolar-Arterial (Aa) oxygenation gradient can be helpful as it may identify the mechanism of hypoxemia

Front 17

R = Respiratory quotient
usually between what numbers?

Back 17

0.7-0.8

Front 18

What is (Predicted) PAO2 on Room air @ sea level?
How do you calculate it?

Back 18

(Predicted) PAO2 = 100 mmHg
Room air @ sea level

1. PiO2 = FIO2 (PB-PH2O)
PiO2 = 0.21 (760 mm Hg- 47 mm Hg)
PiO2 = FIO2 (713 mm Hg)
PiO2 = 150 mm Hg

2. PAO2 = PiO2 – PaCO2/R (R = 0.8 PaCO2 = 40mm Hg)
PAO2 = 150 mmHg – (40 mmHg / 0.8)

(Predicted) PAO2 = 100 mmHg
Room air @ sea level

Front 19

How do you calculate the Aa gradient?

Back 19

1. PiO2 = FIO2 (PB-PH2O)
PiO2 = 0.21 (760 mm Hg- 47 mm Hg)
PiO2 = FIO2 (713 mm Hg)
PiO2 = 150 mm Hg

2. PAO2 = PiO2 – PaCO2/R (R = 0.8 PaCO2 = 40mm Hg)
PAO2 = 150 mmHg – (40 mmHg / 0.8)

(Predicted) PAO2 = 100 mmHg
Room air @ sea level

3. Aa Gradient = PAO2 – PaO2
Determine difference between PAO2 and measured PaO2

Front 20

The difference is Aa Gradient
is due to:

Back 20

Common assessment of oxygenation
Varies with age
Increases with higher PiO2 and FIO2

Front 21

If PAO2 is decreased
could be due to:

Back 21

Ambient O2 is low (alveolar)
Patient is hypo-ventilating (PCO2 also increased
Aa Gradient will NOT be significantly increased

Front 22

If Aa Gradient is increased:

Back 22

Ventilation/Perfusion mismatch
Shunt
A lung, pulmonary vascular problem!

Front 23

If Aa gradient normal it is not a ____ issue

Back 23

pumonary

Front 24

BP, HR and ECG are okay, it is not a ____ issue

Back 24

cardiac

Front 25

What is V/Q Mismatch?
Examples?

Back 25

Represents a spectrum (V/Q = 0 to infinity)
V/Q = 0 = SHUNT
V/Q = ∞ = DEAD SPACE
“In between” = Likely a “Pulmonary” disorder
PaO2 and O2 sats improve with O2 Rx
Clinical examples: Pneumonia, CHF, COPD

Front 26

Shunt

Back 26

Venous blood entering circulation that has NOT had contact with ventilated lung units
V/Q = zero
O2 Rx does NOT correct
Clinical examples Atelectasis, mucous plugging, AV malformations, intra-cardiac shunts, ARDS, CHF

Front 27

Dead Space

Back 27

Ventilated units do not receive circulating blood
V/Q = ∞
O2 Rx variably corrects; increased pCO2 seen
Clinical examples: Pulmonary embolism, ARDS

Front 28

Causes of ARDS = Adult Resp. Distress Syndrome

Back 28

Spectrum of Acute Lung Injury
Bilateral Pulmonary Infiltrates
Severe V/Q mismatch progressing to Shunt
PaO2/FIO2 < 200
Pulmonary Hypertension
Decreased Lung Compliance
Non-cardiogenic pulmonary edema
Mortality about 30% (2006 data)
Ventilator management includes “Lung Protective Strategy”

Front 29

Pulmonary & Extra-pulmonary causes of ARDS

Back 29

1. Pneumonia
2. Aspiration
3. Sepsis/SIRS
4. Inhalational Lung Injury
5. Lung contusion
6. Pancreatitis
7. Fat emboli syndrome
8. Amniotic Fluid Embolus
9 .Massive Transfusion

Front 30

Hypercarbic Respiratory Failure, when this happens?

Back 30

Hypercarbic respiratory failure: PaCO2 > 45-50 mm Hg.
Can be present with hypoxemic respiratory failure

Front 31

Hypercarbic Respiratory Failure
The physiologic basis is

Back 31

Decreased minute ventilation (VE)
Increased Dead Space (decreased effective VE)
Increased CO2 production that is unable to be removed by lungs

Front 32

Common etiologies of Hypercarbic Respiratory Failure

Back 32

Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders [asthma, chronic obstructive pulmonary disease (COPD)].

Front 33

In Hypercarbic Respiratory Failure The pH depends on the level of

Back 33

bicarbonate, which, in turn, is dependent on the duration of hypercarbia.
Relationship:
[H+] = 24 pCO2 / [HCO3]

Front 34

The higher the pCO2
in In Hypercarbic Respiratory Failure

Back 34

pH decrease
Kidneys work to buffer by retaining HCO3
Correction predicted by:
[HCO3] = [(pCO2 - 40)/10] +24 (Acute; <24hrs.)
[HCO3] = [(pCO2 - 40)/3] +24 (Chronic; >24hrs.)
Not complete compensation
As such problem is with ACIDEMIA not pCO2

Front 35

CO2 sensor located in where?

Back 35

Medulla

Front 36

In Hypercarbic Respiratory Failure responds to changes in pH
Problem with this control associated with disorders of CNS Control of breathing as seen in:

Back 36

Idiopathic hypoventilation
Central Sleep apnea
Overdoses with narcotics or sedatives
Hypothyroidism
Metabolic alkalosis (pCO2 rises 10 mmHg for every 15 meq/L rise in plasma HCO3)
Rabies
Ascending spastic paralysis

Front 37

Motor neuron dysfunction can result in

Back 37

decreased respiratory effort and hypercarbic respiratory failure

Front 38

Motor neuron dysfunction can result in decreased respiratory effort and hypercarbic respiratory failure
due to:

Back 38

Spinal cord injury
Tetanus
Tetanaospasmin blocks release of inhibitory NTs
Guillian-Barré Syndrome
Myasthenia Gravis
Antibodies to acetylcholine receptors
Botulism - neurotoxin
Organophosphate poisoning
Inhibition of cholinesterase = paralysis = hypoventilation

Front 39

Other causes of hypoventilation:

Back 39

Muscle fatigue
Myopathies
Metabolic (hypokalemia, hypomagnesemia)
Acidosis

Front 40

Oxygen administration (COPD)

Back 40

Increased dead space
Attenuation of hypoxemic respiratory drive
Haldane effect
Oxygen releases CO2 bound to HgB

Front 41

Hypoxemia results from one of 4 disorders effecting oxygen delivery:

Back 41

Insufficient O2 saturation
Insufficient Hemoglobin
Malfunctioning Hemoglobin
Insufficient circulation (CHF)

Front 42

Hypercarbia is indicative of____

Back 42

Hypercarbia is indicative of a VENTILATORY problem
Can be at a CNS or muscle level

Front 43

There is a spectrum of V/Q mismatch with respect to alveolar/circulatory units:

Back 43

DEAD SPACE reflects NO circulation to units
SHUNT reflects NO ventilation to units

Front 44

Acute Respiratory Failure

Back 44

A clinical situation
Inability of respiratory system to meet the oxygenation, ventilation or metabolic needs of the patient.
Type I = hypoxemic
Type II = hypercarbic

Front 45

Manifestations of Acute Resp. Failure

Back 45

Abnormal Respiratory Rate
Use of accessory muscles
Paradoxical respiratory movement
Altered heart rate, BP
Cardiac arrhythmias
Altered mental status
Cyanosis (Type I)

Front 46

Risk Factors of Acute Resp. Failure

Back 46

Acute Illness
Airway Obstruction (chronic or acute)
Pre-existing illness
Post-operative
Trauma / Inhalational Injuries
Advanced Age
Malnutrition
Morbid Obesity
Substance abuse (ETOH, recreational drugs, intentional and unintentional overdose of Rx, etc.)

Front 47

Assessing Acute Resp. Failure

Back 47

1. Clinical Assessment
2. Assessment of oxygenation
-Color, perfusion, mental status
-BP, HR
-Oxyhemoglobin saturations
- Arterial Blood gas (pO2)
3. Assessment of Ventilation
-Respiratory rate
-Arterial Blood Gas
a. Measures: PO2, PCO2, pH
b. Calculates O2 sat unless using co-oximeter

Front 48

Assessment of potential causes of ARF

Back 48

History and Physical Exam ; Assess primary and secondary causes
Chest X-ray, Chest CT
Labs
ABG
EKG
Other studies as clinical situation dictates

Front 49

Treatment of Acute RF

Back 49

ABC’s = Airway-Breathing-Circulation
Determine if patient needs intubation
Oral intubation best
Assess adequacy of circulation
Begin Mechanical Ventilation = another talk
Chest x-ray to check ET tube placement!
Re-assess oxygenation, ventilation, patient comfort
Assess for Lung Injury – ARDS
ICU care – prevention of secondary issues

Front 50

Causes of Acute RF

Back 50

1. Pulmonary
Chronic Obstructive Pulmonary Disease
Can be hypoxemic, hypercarbic or both
Pneumonia
Asthma
Pulmonary Embolism
ARDS
2, Cardiac
Myocardial Infarction
CHF
3. Neurological
Stroke
Neuromuscular diseases – Myasthenia, GBS
Can be hypoxemic, hypercarbic or both
Head Injury
Acute Neurological deterioration
4. Any Infection – Sepsis – progressing to ARDS
5. Trauma
Pulmonary Contusion
Penetrating injury/Pneumothorax
Near Drowning
6. Airway Obstruction/Foreign Body aspiration

Front 51

Acute Resp. Failure: Rx

Back 51

Goals of Therapy
Stabilize patient
Ventilator management
Optimize pO2
Optimize pCO2 considering patient baseline
Minimize ventilator induced lung injury
Treat underlying disease/precipitating event
If infectious cause = optimal, timely ABX
If ARDS = “Lung protective strategy”

Front 52

Management of RF must take into account

Back 52

OXYGENATION and VENTILATION.

Front 53

Two general groups of patients
in Mechanical Ventilation

Back 53

Full rest is indicated
Where some use respiratory muscles is indicated

Front 54

Some Typical Clinical Indications
for Mechanical Ventilation

Back 54

1. Insufficient oxygenation
Lung dysfunction (pneumonia, CHF, etc)
2. Insufficient ventilation
Decreased level of consciousness
Apnea
3. Clinical need to decrease the work of breathing (i.e. COPD exacerbation)
4. Surgery (elective intubation)

Front 55

What effects CO2 and O2?

Back 55

The greatest determinant of CO2 elimination is minute ventilation (VE):

VE = Tidal volume (Vt) x Resp.rate (R)

The greatest determinants of O2:
The inspired fraction of oxygen (FIO2)
Positive end expiratory pressure (PEEP)

Front 56

The greatest determinant of CO2 elimination is

Back 56

minute ventilation (VE):

VE = Tidal volume (Vt) x Resp.rate (R)

Front 57

The greatest determinants of O2:

Back 57

The inspired fraction of oxygen (FIO2)
Positive end expiratory pressure (PEEP)

Front 58

Ventilator Settings

Back 58

1. Invasive versus Non-invasive
2. Mode = The mechanism of delivery
Volume limited (AC, CMV, IMV)
Pressure limited (PCV)
Flow limited (PSV) – not truly “limited”
Time limited
3. Rate = Breaths per minute
4. Tidal volume (Vt )= Volume per breath
Usually 8-10 cc/kg
5. PEEP = positive end expiratory pressure
6. FiO2 = Fraction of inspired oxygen
7. Inspiratory Flow = how fast Vt delivered
8. Flow pattern = Manner of delivery of the Vt
9. I:E Ratio = may be a default depending on mode

Front 59

Mode” = 3 variables

Back 59

1. Trigger = what initiates the breath
Patient effort = flow or pressure change
Machine timed
2. Target or Limit Variable = what controls delivery
Flow
Inspiratory Pressure
3. Cycle = what Limits or Terminates breath
Volume
Inspiratory Time
Flow rate
Pressure is a back-up safety cycle variable

Front 60

Modes of Ventilation 1 Volume Limited (or Cycled)

Back 60

1. Controlled mechanical (CMV)
2. Assist Control (AC)
3. Intermittent Mandatory Ventilation (IMV)

Front 61

= what initiates the breath in modes of ventilation

Back 61

Trigger in modes of ventilation

Front 62

what controls delivery in modes of ventilation

Back 62

Target or Limit Variable in modes of ventilation

Front 63

what Limits or Terminates breath in modes of ventilation

Back 63

Cycle in modes of ventilation

Front 64

Controlled mechanical (CMV)

Back 64

VE determined entirely by the set respiratory rate and tidal volume (Vt).
Patient does not initiate additional breaths above that set on the ventilator

volume limited modes of ventilation

Front 65

VE determined entirely by the set respiratory rate and tidal volume (Vt).
Patient does not initiate additional breaths above that set on the ventilator

Back 65

Controlled mechanical (CMV)in volume limited modes of ventilation

Front 66

Assist Control (AC)

Back 66

the clinician determines the VE by setting the respiratory rate and tidal volume.
The patient can increase the VE by triggering additional breaths
Tidal Volume is constant for set or initiated breaths

volume limited modes of ventilation

Front 67

the clinician determines the VE by setting the respiratory rate and tidal volume.
The patient can increase the VE by triggering additional breaths
Tidal Volume is constant for set or initiated breaths

Back 67

Assist Control (AC)
in volume limited modes of ventilation

Front 68

Intermittent Mandatory Ventilation (IMV)

Back 68

in volume limited modes of ventilation
Similar to AC: The clinician determines the minimal VE (by setting the respiratory rate and tidal volume)
The patient is able to increase the VE.
Differs from AC in the way that the VE is increased.
Patients increase the VE by spontaneous breathing, rather than patient-initiated ventilator breaths.

Front 69

The clinician determines the minimal VE (by setting the respiratory rate and tidal volume)
The patient is able to increase the VE.

Back 69

Intermittent Mandatory Ventilation (IMV)
in volume limited modes of ventilation

Front 70

Compare IMV and AC volume limited modes of ventilation

Back 70

Similar to AC: The clinician determines the minimal VE (by setting the respiratory rate and tidal volume)
The patient is able to increase the VE.
Differs from AC in the way that the VE is increased.
Patients increase the VE by spontaneous breathing, rather than patient-initiated ventilator breaths.

Front 71

Synchronous Intermittent Mandatory Ventilation (SIMV)

Back 71

in volume limited modes of ventilation
SIMV is a variation of IMV
Ventilator breaths are synchronized with patient inspiratory effort using pressure or flow-by triggering
Tidal Volume may vary.

Front 72

SIMV is a variation of IMV
Ventilator breaths are synchronized with patient inspiratory effort using pressure or flow-by triggering
Tidal Volume may vary.

Back 72

Synchronous Intermittent Mandatory Ventilation (SIMV)
in volume limited modes of ventilation

Front 73

Pressure Limited modes of ventilation

Back 73

Clinician set: the inspiratory (drive) pressure level, I:E ratio, respiratory rate, PEEP, and FiO2.
Inspiration ends after delivery of the set inspiratory pressure.
Vt is variable = related to pressure (P1V1 = P2V2), compliance, airway resistance, tubing resistance
A specific VE cannot be guaranteed!

Front 74

Pressure-limited AC:

Back 74

respiratory rate and inspiratory pressure level determine the minimum VE.
The patient is able to increase the minute ventilation by triggering additional ventilator-assisted, pressure-limited breaths.
Also called Pressure-regulated volume control (PRVC)

Front 75

respiratory rate and inspiratory pressure level determine the minimum VE.
The patient is able to increase the minute ventilation by triggering additional ventilator-assisted, pressure-limited breaths.
Also called Pressure-regulated volume control (PRVC)

Back 75

Pressure-limited AC:
in modes of ventilation

Front 76

Respiratory rate and inspiratory pressure level determine the minimum VE.
The patient is able to increase the minute ventilation by initiating spontaneous breaths

Back 76

Pressure-limited IMV or SIMV

Front 77

Pressure-limited IMV or SIMV

Back 77

Respiratory rate and inspiratory pressure level determine the minimum VE.
The patient is able to increase the minute ventilation by initiating spontaneous breaths

Front 78

Volume versus Pressure Limited modes of ventilation

Back 78

1. No (statistically) significant differences in:
Mortality
Oxygenation
Work of breathing
2. Pressure-limited may be associated with:
lower peak airway pressures
more homogeneous gas distribution
improved patient-ventilator synchrony
earlier liberation from mechanical ventilation
3. Only volume-limited ventilation can guarantee constant Vt and VE

Front 79

Pressure-limited modes of ventilation MAY be associated with: *******

Back 79

lower peak airway pressures
more homogeneous gas distribution
improved patient-ventilator synchrony
earlier liberation from mechanical ventilation

Front 80

Flow Limited Ventilation (Pressure Support -PSV) –

Back 80

not truly a “limited” mode
A preset airway pressure is delivered after the ventilator is triggered. Unpredictable Tidal Volumes
Inspiration ends when the inspiratory flow decreases to a predetermined percentage of its peak value

it is controlled if flow and volume have the same shape

Front 81

A preset airway pressure is delivered after the ventilator is triggered. Unpredictable Tidal Volumes
Inspiration ends when the inspiratory flow decreases to a predetermined percentage of its peak value

Back 81

Flow Limited modes of Ventilation

Front 82

Flow Limited Ventilation (PSV) Clinician sets:

Back 82

Pressure support level (inspiratory pressure level)
Inspiratory flow rate
PEEP
FiO2.

Front 83

Flow Limited Ventilation (PSV) -Concepts

Back 83

NO SET RESPIRATORY RATE or VE!
Patient must trigger each breath.
The Vt, respiratory rate, and VE are dependent on multiple factors (ventilator settings, compliance, sedation) – THESE VARY!
In general, a high pressure support level results in large Vt and a low respiratory rate.
Patient should have spontaneous breathing
Often used as a “weaning mode” – but SBTs may be better

Front 84

Flow Limited Ventilation (Pressure Support) – Caveats

Back 84

Each breath must be initiated by the patient
An adequate minute ventilation cannot be guaranteed because tidal volume and respiratory rate are variable
Ventilator asynchrony can occur
PSV is associated with poorer sleep than AC.
Relatively high levels of pressure support (>20cm H2O) are required during full ventilatory support to prevent alveolar collapse

Front 85

Continuous Positive Airway Pressure (CPAP)

Back 85

delivery of a continuous level of positive airway pressure.
Functionally similar to PEEP.
No additional pressure above the level of CPAP is provided
Patients must initiate all breaths

Front 86

delivery of a continuous level of positive airway pressure.
Functionally similar to PEEP.
No additional pressure above the level of CPAP is provided
Patients must initiate all breaths

Back 86

Continuous Positive Airway Pressure (CPAP)

Front 87

Bi-Level Positive Airway Pressure (Bi-PAP®)

Back 87

Used during noninvasive positive pressure ventilation (NPPV).
Delivers a preset inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP).

Front 88

Used during noninvasive positive pressure ventilation (NPPV).
Delivers a preset inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP).

Back 88

Bi-Level Positive Airway Pressure (Bi-PAP®)

Front 89

Airway Pressure Release

Back 89

High continuous positive airway pressure (Phigh) is delivered for a long duration (Thigh) and then falls to a lower pressure (Plow) for a shorter duration
Spontaneous breathing is possible
No universally accepted indications – may be good for patient with elevated Intracranial pressure?

Front 90

High continuous positive airway pressure (Phigh) is delivered for a long duration (Thigh) and then falls to a lower pressure (Plow) for a shorter duration
Spontaneous breathing is possible
No universally accepted indications – may be good for patient with elevated Intracranial pressure?

Back 90

Airway Pressure Release

Front 91

Mechanical Ventilation - ARDS

Back 91

1. Employ “lung protective” strategy
ARDSNET Trial25
9% decrease in all cause mortality
Vt of 6 ml/kg (as opposed to 12 ml/kg)
Plateau Pressure < 30 cm H2O
2. Permissive hypercapnia may be required
Shown to be safe (small nonrandomized series)
Safe in ARDSNET trial, but was not clinical endpoint25
Existing metabolic acidosis may limit use
Contraindicated in patients with increased ICP

Front 92

Mechanical ventilation can be

Back 92

be invasive or noninvasive.

Front 93

The physiological benefits of mechanical ventilation are

Back 93

improved gas exchange and decreased work of breathing

Front 94

Mechanical ventilation is indicated for

Back 94

for acute or chronic respiratory failure, defined as insufficient oxygenation, insufficient alveolar ventilation, or both

Front 95

Once it has been determined that a patient requires mechanical ventilation the clinician must choose

Back 95

the mode, the amount of support, and the initial ventilator settings

Front 96

In setting of ARDS, a lung protective strategy should be employed to

Back 96

minimize volume induce lung injury as this has been shown to decrease mortality in the ARDSNET trial.