Chapter 41
Respiratory Failure and the Need for
Ventilatory Support
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Learning Objectives




Define acute respiratory failure.
Differentiate between hypoxemic (type I) and
hypercapnic (type II) respiratory failure
Discuss the causes of acute respiratory
failure.
Contrast chronic respiratory failure and acuteon-chronic respiratory failure.
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Learning Objectives (cont.)




Identify the complications of respiratory
failure.
Discuss the indications for ventilatory support.
Describe the general management principles
of hypoxemic and hypercapnic respiratory
failure.
Discuss the indications for noninvasive
ventilation.
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Introduction: Respiratory Failure


Inability to maintain oxygen delivery to tissues
or adequate removal of carbon dioxide from
body
Criteria




PaO2 < 60 mm Hg and/or
PaCO2 > 50 mm Hg
In individuals on room air at sea level
36% hospital mortality
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Hypoxemic Respiratory Failure
(Type I)

Causes
of hypoxemia
. .

V/Q mismatch (most common cause)
 Shunt
 Alveolar hypoventilation
 Diffusion impairment
 Perfusion/diffusion impairment (rare)
 Decreased inspired oxygen
 Venous admixture
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All of the following are causes of hypoxemia,
except?
A.
B.
C.
D.
Shunt
Alveolar hyperventilation
Diffusion impairment
Decreased inspired oxygen
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. .
V/Q Mismatch
. .

Normal. physiology
V/Q
.



High V/Q at apices of lung
. .
Low V/Q at bases of lung
. .
Disease worsens V/Q mismatch impairing
ventilation, while perfusion remains adequate

Obstructive lung disease (asthma, COPD)
 Infection, heart failure, inhalation injury
• Partially collapsed or fluid-filled alveoli
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. .
V/Q Mismatch (cont.)
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Clinical Presentation


Patient has low PaO2 & SaO2
Presents with

Nonspecific: dyspnea, tachycardia, tachypnea
 Accessory muscle use (important sign)
 Nasal flaring
 Pedal edema (RF is cardiac in origin)
 Cyanosis (peripheral or central)
 Confusion to coma if CNS dysfunction
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Clinical Presentation (cont.)

Auscultation



. .
V/Q
Bilateral wheezing
• Bronchospasm, fluids, or upper airway disease
Breath sounds diminished bilaterally
• Common finding with emphysema
Unilateral abnormalities important
• Wheezing one lung may signify lesion
• Absence of B/S one lung: collapse, effusion
• Unilateral crackles: alveolar filling process
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Clinical Presentation (cont.)

Radiographically can present as “black” or
“white”

Black radiograph
• Hyperinflated lungs characteristic of obstructive lung disease
 White radiograph
• Evidence of partial or total alveolar filling
• Characteristic of restrictive lung disease
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Shunt


Normal anatomic shunt ~2-3% of cardiac output
Pulmonary shunt occurs when NO ventilation to
match perfusion



Always pathologic
Leads to hypoxemia as alveoli collapse or filled with
fluid or exudate
• Atelectasis, pulmonary edema, pneumonia
Major difference between shunt &
mismatch
. .
V/Q
. .
 V/Q mismatch responds to oxygen therapy unlike
shunt which is refractory
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Which of the following is the major difference
between of V/Q mismatch and a shunt?
A. V/Q mismatch responds to oxygen therapy unlike
shunt which is refractory
B. Shunt responds to oxygen therapy unlike V/Q
mismatch which is refractory
C. Pulmonary shunt occurs when there is ventilation
to match perfusion
D. Shunt leads to hyperxemia as alveoli collapse
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Shunt (cont.)
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Clinical Presentation

Shunt presents very similar to



. .
V/Q
mismatch
Usually presents with white radiograph
• ARDS is classic example
. .
mismatch often presents with black radiograph
V/Q
. .
V/Q
Differentiated from
mismatch by lack of
response in PaO2 as FIO2 is increased
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Diffusion Impairment


Most pronounced on exertion
Impairment can be caused by




Thickened/scarred: fibrosis, asbestosis
Alveolar destruction: emphysema
Pulmonary vascular abnormalities
• Anemia, pulmonary emboli or hypertension
Clinical presentation depends on disease


Dry cough, fine bibasilar cracklespulmonary
fibrosis
Jugular distention, edemapulmonary hypertension
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Decreased Inspired Oxygen

Clinically uncommon


High altitude while mountain climbing
Airlines pressurized cabins but not to 1 atm
• Travelers with pulmonary disease may require
supplemental oxygen or more supplemental oxygen than
normal

Signs & symptoms of hypoxemia may present

Treat with oxygen
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Venous Admixture



Decreased mixed venous oxygen
Clinically patient’s lung must add more oxygen
to blood; presence of pulmonary disease may
prevent
Heart failure is most common cause


Decreased cardiac output: tissues extract more
oxygen
Clinically presents with signs & symptoms of
CHF and/or underlying pulmonary disease
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Differentiating Between Causes of
Hypoxemic Respiratory Failure

Focus on three main causes:



Hypoventilation
• Normal P(A  a)O2: 1025 mm Hg
. .
V/Q mismatch
• Significant response to oxygen therapy
Shunt
• Little or no improvement even on 100% O2
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Which of the following is a form of hypoxemia that
would occur in the face of a normal P(A – a)O2
A.
B.
C.
D.
Shunting
V/Q mismatch
Hyperventilation
Hypoventilation
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Hypercapnic Respiratory Failure
(Type II)


aka “pump failure” or “ventilatory failure”
Elevated PaCO2 results in uncompensated
respiratory acidosis
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Hypercapnic Respiratory Failure
(Type II) (cont.)

PaCO2 & alveolar ventilation are inversely
proportional. Mathematically:
.
PaCO2 = (0.863 VCO2)/ V A
.
A = MV (1  VD/VT)
VA = alveolar ventilation; VCO2 = CO2 production
MV = minute volume; VD/VT = dead space-to-tidal
volume
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Impairment in Respiratory Control

Ventilatory drive most commonly diminished by:







Drug overdose or sedation
Brainstem lesions
Diseases of CNS
• Multiple sclerosis or Parkinson’s disease
Hypothyroidism
Morbid obesity
Sleep apnea
Clinical hallmark is bradypnea (<12 beats/min) &
ultimately apnea
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Impairment in Respiratory Effectors

Neurologic Diseases

CNS signals fail to reach ventilatory muscles due
to:
• Spinal trauma
• Motor neuron disease (ALS or polio)
• Motor nerve disorders (GBS)
• Neuromuscular junction disorders (MG or botulism)
• Muscular diseases (MD, myositis)
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Clinical Presentation

Varied presentation




Drooling, dysarthria, weak cough - ALS
Lower extremity weakness progressing upward – GBS
Ocular muscle weakness, ptosis, diplopia, dysphagia –
Myasthenia gravis
Different clinical presentations, yet commonly
result in respiratory muscle fatigue & ventilatory
failure (elevated CO2)
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Increased Work of Breathing

Ventilatory failure may occur if imposed
workload cannot be overcome

Most commonly occurs secondarily to
• Increased VD/VT in COPD
• Elevated Raw in asthma
• Both cause intrinsic PEEP, which generates excessive
WOB

May also be caused by
• Pneumothorax, rib fractures, pleural effusions
• Hypermetabolic states such as burns
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Clinical Presentation

Rapid shallow breathing is indication of
impending ventilatory failure




Shallow breathing increases VD/VT ratio & results in
hypercapnia
Diminished B/S in young asthmatic is ominous
not moving adequate air
Irritability, confusion, & coma are signs of
worsening hypercapnia
Muscle tremors & papilledema
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Chronic Respiratory Failure
(Type I & Type II)



Over months & years, acute respiratory failure
will become chronic condition
Body develops compensatory mechanisms
Chronic type I failure (hypoxemic)



Polycythemia & oxy-Hb shift to right
Cerebral blood flow enhanced by increased PaCO2
Chronic ventilatory failure (hypercapnic)

Renal response: retain HCO3 to normalize pH
• Will be incomplete but will raise pH toward normal
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All of the following are clinical presentations of
worsening respiratory failure, except?
A.
B.
C.
D.
Decreased VD/VT ratio
Diminishing breath sounds
Irritability, confusion, and coma
Muscle tremors and papilledema
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Acute-on-Chronic Respiratory Failure


Chronic failure complicated by acute failure
Most commonly brought about by





Bacterial or viral infections
CHF
Pulmonary embolus
Chest wall dysfunction
Medical noncompliance
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Acute-on-Chronic Respiratory Failure
(cont.)


49% mortality within 2 years of acute
exacerbation
Key: Treat aggressively to prevent further
exacerbations
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Complications of Acute Respiratory
Failure

Complications add significantly to morbidity &
mortality



ARDS- more patients die of complications (sepsis,
MSOF) than of original disease
Emboli, barotrauma, & infection common
Nonpulmonary complications include
• Cardiac: arrhythmias, hypotension
• Gastrointestinal: hemorrhage, dysmotility
• Renal failure and/or positive fluid balance
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Clinical Presentation of Acute
Respiratory Failure

Respiratory muscle fatigue presents




Tachypnea: cardinal sign of increased WOB
Worsening fatigue RR starts falling, bradypnea
occurs, & apnea
Respiratory alternans
Full ventilatory failure

ABG: hypercapnia with acidosis
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Indications for Ventilatory Support

Goal of MV is constant

Supportive therapy until underlying problem
resolves
Provide long-term support for patients with chronic
ventilatory failure
Support aimed at patient’s specific needs


•
ARDS patient’s ventilatory needs will differ markedly from
patient with C1 spinal cord injury
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Indications for Ventilatory Support
(cont.)
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Hypoxemic Respiratory Failure

Refractory hypoxemia is common indication for
intubation & MV


Indices to assess need include:
• P(A  a)O2 > 350 on 100% oxygen
• P/F ratio (PaO2/FIO2) < 200
Frequently, hypoxemic and hypercapnic
respiratory failure occur simultaneously
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Hypercapnic Respiratory Failure

Elevated PaCO2 may or may not indicate
need for ventilatory support

PaCO2 > 55 with pH < 7.20; acute process
probably requires ventilation

PaCO2 > 55 with pH near normal; chronic failure
with renal compensation probably does not require
MV

The trend for PaCO2 & pH is very useful
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Significance of an Elevated PaCO2
.
V CO2

Normally increased
is matched by
.
increased V A so PaCO2 should not change

Elevated PaCO2 indicates 1 of 3 problems
1.
2.
3.
Respiratory center dysfunction
Nerve transmission problems
Lungs & chest are incapable of providing
adequate ventilation due to disease or weakness
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Assessment of Respiratory Muscle
Weakness


Commonly occurs in neuromuscular disease
(NMD) patients, but also COPD & kyphoscoliosis
Tests to assess respiratory muscle strength

MIP of >20 is inadequate, but watch trends
 In NMD trend of MIP becoming less negative
indicates impending ventilatory failure

VC & MMV have limited value in ICU setting as
patients are generally too SOB to cooperate
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Respiratory Muscle Weakness,
Fatigue, & Failure



Weakness, fatigue, & failure overlap & may
result in acute or chronic failure
Excessive WOB is most common cause of
respiratory muscle fatigue & failure to wean from
MV
Imposed WOB in ventilated patients due to:





ETT
Ventilator circuit
Auto-PEEP
Disease process
If patient’s WOB is <0.8 J/L, 96% successfully
extubate
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All of the following can increase WOB on
ventilated patients, except:
A.
B.
C.
D.
Artificial airway
Ventilator circuit
Pressure support
Underlying pulmonary disease
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Ventilatory Support Strategy: NIV


Noninvasive ventilation provides support without
intubation
Types of NIV include

CPAP
 Pressure support ventilation
 Volume ventilation (A/C or SIMV)
 Pressure ventilation (A/C or SIMV)
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Ventilatory Support Strategy: NIV
(cont.)

Clinical situations that may respond to NIV

Acute exacerbations of COPD (good evidence)
 Cardiogenic pulmonary edema (reversibility)
 Acute asthma (use is controversial)
 Acute type I failure: improved P/F ratio but no patient
important outcomes (i.e., LoS, M/M)
 Chronic type II failure particularly NMD: improves &
prolongs life & cognitive function; reduces pneumonia
& hospitalization
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Invasive Ventilatory Support

IPPV indicated for



Severe hypoxemia caused by disease that is slow
to resolve, i.e., ALI
Patients needing support who cannot tolerate or
are contraindicated for NPPV
Effective for hypoxemic & hypercapnic respiratory
failure
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Ventilatory Support: ARDS


Patients have very noncompliant lungs
Best to ventilate patients with small VT (~6
ml/kg)


This strategy
• Reduces complications
• Improves survival
Often use permissive hypercapnia strategy

Allow CO2 to slowly rise, maintaining pH > 7.2 to
7.25
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Ventilatory Support: Head Injury

Ventilation patients with increased ICP

Short term can hyperventilate (PaCO2 25 to 30 mm
Hg) to alleviate spikes in ICP
 Long term support: PaCO2 30 to 40 mm Hg
 PEEP may increase CVP, deceasing pressure
gradient for cerebral venous drainage which in turn
elevates ICP
• Alleviate affects by raising head of bed
• If patient is unstable, may require invasive ICP monitoring
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Ventilatory Support: COPD

Ventilator settings optimized

Low VT of 6 to 8 ml/kg IBW
 Moderate RR
 High inspiratory flow rates (70 to 100 L/min)
 These reduce IT, prolong ET
• These minimize auto-PEEP
 Set PEEP to alleviate imposed WOB &
asynchrony associated with auto-PEEP
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Ventilatory Support: Chronic
Ventilatory Failure


Goal is to normalize pH but not PaCO2
If PaCO2 is normalized, may cause


Metabolic alkalosis, which can produce
• Hypokalemia
• Seizures
• Arrhythmias
May prolong weaning from mechanical ventilation
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All of the following can occur if PaCO2 is
normalized in patients with chronic respiratory
failure, except?
A.
B.
C.
D.
Metabolic acidosis
Hypokalemia
Seizures
Arrhythmias
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