Download Type II Respiratory Failure

Type II Respiratory Failure
COPD and Status Asthmaticus
Outline
1.
COPD
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Pathophysiology
Dynamic Hyperinflation
Approach to the Patient
Status Asthmaticus
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Pathophysiology
Presentation
Therapy
Chronic Obstructive
Pulmonary Disease
Acute on Chronic Respiratory
Failure
Pathophysiology
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Alveolar ventilation is maintained by the CNS,
which acts through nerves and the respiratory
muscles.
The three subsets of ventilatory failure are loss
of drive, impaired neuromuscular competence,
and excessive load.
Few patients have a loss of drive and usually
occurs in the setting of drug/alcohol overdose or
physician-directed sedation.
Pathophysiology
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Inspiratory muscle fatigue is the primary
mechanism.
A muscle fatigues when its energy consumption
exceeds that supplied by blood flow.
In an acute exacerbation, respiratory muscle
oxygen consumption can rise to 17-46% of total
body consumption.
The most significant contributor to elastic load is
dynamic hyperinflation.
Dynamic Hyperinflation
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Airflow obstruction prolongs expiration.
When the rate of alveolar emptying is slowed,
expiration cannot be completed before the next
inspiration.
Therefore, the lung fails to reach FRC at the end
of each breath and there remains a positive
elastic recoil pressure which is called intrinsic
PEEP (PEEPi).
Greater effort must be generated to initiate a
breath due to the PEEPi.
Dynamic Hyperinflation
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At the same time that the load is
increased, the respiratory muscles are
forced to operate in a disadvantageous
position of the force-length relationship.
Diaphragm strength is only 2/3 normal in
stable COPD patients which is due
diaphragm position and not inherent
muscle weakness.
Dynamic Hyperinflation
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Patients with dynamic hyperinflation also
frequently have other conditions such as
malnutrition and steroid induced myopathy that
causes intrinsic muscle weakness.
Patients with severe COPD live a balanced life
between increased load and diminished
neuromuscular competence.
Any minor decrement in strength or increase in
load are enough to precipitate muscle fatigue
and respiratory failure.
Other Causes of Increased Load
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Resistive load
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Airway resistance is increased by
bronchospasm, airway inflammation,
and mucous plugging.
Superimposed heart failure may also
increase airway resistance.
Tracheal stenosis should be considered
in patients with previous intubations.
Sleep-disordered breathing commonly
coexists with COPD also needs to be
excluded.
Other Causes of Increased Load
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Increased lung elastic load
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Pulmonary edema, pneumonia, interstitial
fibrosis, tumor, and atelectasis all contribute
to increased lung stiffness.
Minute ventilation load
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An increase in CO2 production from caloric
intake, fever, agitation, muscular exertion,
and hypermetabolism from injury or
inflammation imposes a higher excreation
load.
Worsened dead space may be caused by
pulmonary embolism, hypovolemia, PEEP, or
shallower breathing (raises the dead space
fraction, Vd/Vt)
Approach to the Patient: Early
Acute on Chronic Failure
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The goal in the patient not yet intubated is to
avoid mechanical ventilation when possible and
to recognize progressive respiratory failure when
it is not.
NIPPV is a proven therapy that can avert
intubation in up to 75% of patients with ACRF.
It is not a cure but buys the physician time to
treat the precipitants of ACRF and for the patient
to improve.
Current guidelines recommend NIPPV as first-line
therapy for COPD-related acute on chronic
respiratory failure (ACRF).
Approach to the Patient: Early
Acute on Chronic Failure
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NIPPV has been shown to relieve
symptoms, reduce respiratory rate,
increase tidal volume, improve gas
exchange and reduce diaphragmatic
work.
Complications are few and minor; local
skin breakdown from the mask is simple
to treat.
Careful patient selection is essential for
successful NIPPV.
Selection Criteria for NIPPV
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Establish need for assistance
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Moderate/severe respiratory distress
Tachypnea
Use of accessory muscles
pH<7.35, PaCO2>45, or P/F ratio<200
Exclusions
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Respiratory arrest
Medically unstable
Unable to protect airway
Excessive secretions
Severe agitation
Unable to fit mask
Recent upper airway or GI surgery
NIPPV
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A risk of NIPPV is its potential to lull the team
into a sense of comfort while the patient
continues to worsen.
Time spent trying NIPPV may potentially lead to
a later, more urgent intubation in an exhausted
patient with greater tissue hypoxia.
Avoiding intubation is always dependant on
discerning the cause of ACRF and reversing it.
Oxygen
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One of the greatest myth of mankind is that
patients rely on hypoxic drive to breathe.
As a result, oxygen is withheld and the
underlying hypoxia is left untreated.
This leads to worsening acidemia, fatiguing
respiratory muscles, failing right ventricle,
arrhythmias, myocardial ischemia, cerebral
injury, and respiratory arrest.
Oxygen
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When oxygen is given, the PCO2 may rise but
this is due to worsened V/Q matching and the
Haldane effect, not to hypoventilation.
The goal of oxygen therapy is to maintain 90%
saturations which can usually be attained with 35 L/min.
Patients may still progress to respiratory failure
despite oxygen therapy, but not because of it.
Pharmacotherapy
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Bronchodilators are an essential part of
the management even though most of the
airflow obstruction is irreversible as most
patients have some reversible component.
Inhaled B2-selective agents should be
given by MDI with spacer unless patient
distress makes that impractical in which
case a nebulizer may be used.
Pharmacotherapy
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The addition of ipratropium yields increment benefit in
patients with stable COPD but does not result in
improved bronchodilation in acute exacerbation.
Patients given steroids demonstrate improvement within
12 hours.
Current guidelines recommend methylprednisolone 0.5-1
mg/kg every 6 hours during the acute exacerbation with
a transition to oral therapy when tolerated.
Bacterial bronchitis is a common precipitant of ACRF and
appropriate coverage for CAP should be started
empirically.
Recognizing Impending Respiratory
Failure
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Some patients will progress to frank respiratory failure
despite aggressive attempts to find and reverse the
causes.
The decision to intubate requires clinical judgment and is
best assessed by the physician present AT THE
BEDSIDE.
Assessment of respiratory failure based solely on results
of ABGs is fraught with errors.
Useful bedside parameters include increasing respiratory
rate (despite NIPPV), decreasing mentation, pattern of
breathing (abdominal paradox and respiratory
alternans), and the patient’s own assessment
Peri-intubation Risks
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There are two pitfalls in the postintubation period:
hypotension and alkalosis.
Hypotension is a consequence of increasing PEEPi
following intubation resulting from manual
hyperinflation.
PEEPi reduces venous return which is aggravated by
reduced preload and right heart dysfunction.
In addition, the medications used during intubation
have vasodilatory and sympatholytic properties.
The circulation can be restored by holding ventilation
for 30 seconds (to reduce PEEPi) in addition to volume
and bolus vasopressors as needed.
Peri-intubation Risks
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Most patients have a minute ventilation of 10 L/min and
tidal volume of 300 mL.
Higher minute ventilation can occur during bagging and
inappropriate ventilator settings.
This cause the PaCO2 to be driven down in combination
with a pre-existing compensatory metabolic alkalosis
that produces a sever metabolic alkalosis.
This is further aggravated by a fall in VCO2 from resting
respiratory muscles.
This combination can easily produce a pH >7.7 which is
life threatening.
Improving Neuromuscular
Competence
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Malnutrition is a common comorbidity of advanced COPD
and may contribute to respiratory muscle dysfunction.
However, excessive refeeding can cause high levels of CO2
production and should be avoided.
Once the muscles are rested, a program of exercise should
be initiated in conjunction with daily readiness for
liberation from mechanical ventilation screens.
The goal is to encourage muscle power, tone and coordination by allowing the patient to assume nonfatigueing
respirations.
After a period of work, the patient is returned to full rest
on the ventilator to facilitate sleep.
As strength improves, the amount of exercise is increased
until the patient is liberated from the ventilator.
Decreasing Load
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It is important to continue treatment with
bronchodilators either with nebulizers or
MDI.
Other contributors to increased load such
as CHF, PE, and pneumonia should be
sought and treated.
Status Asthmaticus
Characteristics
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Asthma is characterized by wheezing,
dyspnea, cough, hyper-reactive airways,
and reversible airflow obstruction.
Usually, an exacerbation is managed
uneventfully in an ambulatory setting.
However, severe attacks and death can
occur regardless of disease classification
and sometimes with little warning.
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Severe asthma is defined as:
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Dyspnea at rest
Upright positioning
Inability to speak in phrases or sentences
Respiratory rate > 30
Use of accessory muscles
Pulse > 120
Pulsus paradoux > 25 mmHg
Peak expiratory flow rate < 50% predicted
Hypoxemia
Eucapnia or hypercapnia
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Imminent respiratory failure is marked by:
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Altered mental status
Paradoxical respirations
Bradycardia
Quiet chest
Absence of pulsus paradoxus
Pathophysiology
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Exacerbations often evolve over hours to
days before patients seek medical care.
Airway inflammation leads to plugging of
large and small airways with tenacious
mucus.
Mucus plugs consists of sloughed epithelial
cells, eosinophils, and fibrin that leak
through the denuded epithelium.
Pathophysiology
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Smooth muscle bronchospasm occurs in all
patients but a small subset have a sudden onset
with intense spasm and little inflammation.
This is can be lethal but also can also improve
rapidly with bronchodilators.
Triggers include NSAIDS, B-blockers, allergens,
exercise, stress, sulfites, and cocaine.
Respiratory tract infections are not a usual
trigger.
Gas Exchange Abnormalities
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Airway obstruction causes V/Q mismatch.
Shunting is trivial so small amounts of oxygen
corrects hypoxemia.
Refractory hypoxia is rare and suggests
additional pathology.
As the severity of obstruction increases, the
PaCO2 rises due to inadequate alveolar
ventilation and increased CO2 production from
the respiratory muscles.
The absence of hypercapnia does not preclude a
severe attack nor the potential for respiratory
arrest.
Circulatory Effects of Severe Airway
Obstruction
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High intrathoracic pressures during expiration:
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Vigorous inspiration:
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Augments RV filling
Shifts the septum into the left ventricle
Diastolic dysfunction
Incomplete LV filling
Impaired LV emptying
Lung hyperinflation:
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Decrease right-sided preload
Increases RV afterload
Transient pulmonary hypertension
This is the basis for pulsus paradoxus.
Clinical Presentation: Medical
History
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Characteristics of prior exacerbations that can
predict fatal or near fatal episodes include:
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Intubation
Hypercapnia
Barotrauma
Hospitalization despite steroids
Psychiatric illness
Medical noncompliance
Intubation is the greatest single predictor of
death.
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Other concerning features are long symptom
duration, late arrival to care, fatigue, altered
mental status, sleep deprivation.
The absence of a history of asthma should
prompt a search for other diagnoses:
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COPD
CHF
Foreign body aspiration
Upper airway obstruction
Pneumonia
PE
Clinical Presentation: Physical Exam
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The posture, pattern of speech, positioning, and level of
alertness is the best marker of patient condition and
response to therapy.
Airflow obstruction is determined by PEFR and is a good
way to assess and follow patients.
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< 50% predicted or personal best indicates a severe
exacerbation
Hypercapnia on ABG indicates impending respiratory
failure.
Anion gap acidosis is usually due to excess lactate from
increased work of breathing and tissue hypoxia.
Front Line Therapy
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Inhaled B-agonists should be started immediately and
aggressively.
Frequently, higher doses are needed.
Long acting B-agonists are not indicated in initial
treatment.
Subcutaneous administration is not indicated unless the
patient is unable to carry out inhaled therapy but is
associated with greater toxicity.
SC epinephrine may be beneficial in non-responders.
MDI with spacer and nebulizer are equally effective in
delivering treatment.
Combination therapy with ipratropium and albuterol
results in greater bronchodilation compared to either
alone.
Front Line Therapy
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Systemic steroids should given quickly on
initial presentation.
Oral (prednisone 80 mg) or IV
(methylprednisolone 125 mg) routes are
equally effective, but oral should be
avoided if intubation is an issue.
There is no added benefit of inhaled
steroids during the acute phase.
Other Therapies
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Magnesium: May be beneficial in severe attacks but the
jury is still out.
Leukotriene modifiers: Preliminary data suggests benefit
in acute attacks.
Heliox: Less dense so reduces turbulent flow to improve
gas delivery. May mask worsening obstruction so there
is less time and margin for error when intubation
required.
Antibiotics: Infectious triggers are rare so antibiotics
likely have no role.
NIPPV: Decreases work of breathing and may prevent
some intubations.
Intubation
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The goals of intubation are to maintain oxygenation and
prevent respiratory arrest.
40% of deaths in ventilated asthmatics are due to
cerebral anoxia from respiratory arrest prior to
intubation.
Changes in posture, mental status, speech, accessory
muscle use, and respiratory rate indicate failure better
than an ABG or PEFR.
The decision to intubate is best made by a clinician at
the bedside based on their estimation of the patient’s
ability to maintain spontaneous respiration.
Postintubation Hypotension
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Hypotension occurs in 30% of patients and has
several causes:
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Loss of sympathetic tone from sedation
Prehospitalization hypovolemia
Dynamic hyperinflation (DHI) from overzealous
bagging
DHI can be confirmed by a trial of hypopnea.
Improvement after this trial does not exclude
tension pneumothorax (responsible for 6% of
ventilated asthmatic deaths).
Summary
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COPD exacerbations are often multi-factorial in origin.
NIPPV is proven to reduce risk of intubation and
mortality.
Asthma attacks can be sudden and lethal even in
patients with no past history of severe attacks.
40% of deaths in asthma are due to anoxia in the periintubation phase. Do not delay intubation if it appears
inevitable.
Consider dynamic hyperinflation as a cause for postintubation hypotension.