肺部急症
署立桃園醫院
胸腔內科
李世偉 醫師
前言
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
定義
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溺死 ( drowning ):溺水後當場或24小時內死亡
溺水 ( near drowning ):溺水後存活超過24小
時
Submission:所有溺水者,不論預後好壞通稱之
濕溺 ( wet drowning ):溺水時,有明顯液體吸
入
乾溺 ( dry drowning ):溺水時,約有10%的人因
喉部反射使喉不緊閉,造成窒息,沒有吸入液體
病理生理學
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缺氧
水分吸入:淡水及海水
淡水屬於低張力液體, 引起血容量增加,血液稀
釋,電解質濃度減少,紅血球融解造成高血鉀症.
海水屬於高張力液體, 引起血容量減少,血液濃
縮,電解質濃度增加,導致肺水腫.
喉部痙攣
繼發性溺水:約2-5%的溺水者,胸部X光可能為正
常,但在24小時後會發生遲發性的肺水腫,引起呼
吸窘迫症候群.
治療
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心肺復甦術:越早做越好,要注意頸椎的保
護.
氧氣治療
人工呼吸器及PEEP
預防性的抗生素及類固醇並不一定需要,但
如有肺炎發生應給予抗生素治療.
預後
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水溫
年齡
水的污染程度
心臟停止時間及開始心肺復甦術時間
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
Pathophysiology
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Thermal injury
Chemical injury
Hypoxia
Bronchiolitis obliterans organizing pneumonia caused
by inhalation of oxides of nitrogen in a silo filler.
Organizing pneumonia after sulfur dioxide
intoxication.
Diffuse alveolar damage caused by anhydrous ammonia
inhalation. An agricultural worker inhaled the gas when a hose
broke during the transfer of this fertilizing agent.
Radiographic changes produced by diffuse alveolar damage.
Chest radiograph of the same patient as in Figure 66-4 shows
acute, diffuse alveolar and interstitial infiltrates.
Treatment
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High concentration oxygen
Bronchodilator
Adequate fluid therapy
Intubation if upper airway obstruction
Ventilator with PEEP
Antibiotics
Prophylactic steroid is not necessary
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
一氧化碳中毒(CO intoxication)?
Carbon Monoxide
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nonirritating, colorless, tasteless, and odorless
gas
incomplete combustion of carbon-containing
material
occurs in the setting of smoke inhalation,
attempted suicide from automobile exhaust,
and poorly ventilated burning charcoal or gas
stoves
Pathophysiology
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Carbon monoxide binds to hemoglobin with
an affinity that is 240 times greater than
oxygen and decreases oxyhemoglobin
saturation and blood oxygen-carrying capacity.
Its toxicity results from a combination of
tissue hypoxia and direct inhibition of cellular
respiration through cytochrome oxidase
blockade.
Clinical Manifestation
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The severity of carbon monoxide poisoning depends
on the concentration of carbon monoxide, duration
of exposure, and minute ventilation
Carboxyhemoglobin concentrations up to 5% may
result in headache and mild dyspnea.
Carboxyhemoglobin concentrations between 10%
and 30% cause headache, dizziness, weakness,
dyspnea, irritability, nausea, and vomiting.
Carboxyhemoglobin concentrations > 50% result in
coma, seizures, cardiovascular collapse, and death.
Diagnosis
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high index of suspicion for carbon monoxide
poisoning
Important historical clues can aid in the diagnosis.
Carboxyhemoglobin levels are determined by COoximetry.
Pulse oximetry cannot distinguish
carboxyhemoglobin from oxyhemoglobin at the
wavelengths that are commonly generated by
standard pulse oximeters.
Treatment
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The most essential treatment for carbon monoxide
poisoning is oxygen
Administration of 100% supplemental oxygen
decreases the half-life of carboxyhemoglobin from 5
to 6 h on room air to 40 to 90 min.
Hyperbaric oxygen (2.8 atmospheres within 6 h of
exposure) further decreases the half-life of
carboxyhemoglobin to 15 to 30 min.
The role of hyperbaric oxygen in the management of
carbon monoxide poisoning has been debated, and
reviewed.
Prognosis
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10 to 30% of survivors acquire delayed
neuropsychiatric sequelae (DNS).
DNS has been described to occur from 3 to 240 days
after apparent recovery.
Its variable manifestations include persistent
vegetative state, Parkinsonism, short-term memory
loss, behavioral changes, hearing loss, incontinence,
and psychosis.
At 1 year, 50 to 75% of patients with DNS
experience a full recovery.
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
Bleb
Bulla
Pneumothorax
Pneumothorax
Pneumothorax
Characteristics of pnx on supine film
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Pnx easily missed on supine films
(32%)
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Features:
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Increased radiolucency at lung bases
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Sharp, elongated costophrenic/
cardiophrenic sulcus (deep sulcus)
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Depression of hemidiaphragm
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Flattening of heart border
When to Suspect PNX in
Ventilated Patients
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Clinical change in pt’s status
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Sudden or progressive increase in PIP
Hypotension or cardiovascular collapse
Sudden onset of agitation and resp distress
(fighting the ventilator)
CXR findings
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General increase in volume or increase in
relative radiolucency of hemithorax
Deep sulcus sign
Risk Factors for Alveolar Rupture
During MV
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Right main bronchus intubation
High peak inflation volume
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Excessive tidal volume
Excessive PEEP
Auto-PEEP
Obstructive lung diseases (COPD,
Asthma)
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Heterogeneous lung disease
Nosocomial pneumonia
Late phase of ARDS
Steps to Reduce Alveolar Rupture
During MV
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Use small TV
Decrease TV as PEEP increases
Use PEEP cautiously in high risk pt
Avoid right main bronchus intubation
Monitor for auto-PEEP
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High inspiratory flowrate with low I:E ratio
Bronchodilator if bronchospasm is present
Reduce minute ventilation
Chest decompression
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
Life-threatening hemoptysis
According to Coss-Bu et al., major hemoptysis
comprises large and massive bleeding, which
correspond to blood expectoration of 150-400 mL
per day and to more than 400 mL per day,
respectively.
Other definitions of massive hemoptysis range from
400 to 1000 mL per day
Regardless of the exact amount of blood loss for
each category of major hemoptysis, large and
massive hemoptysis are both life-threatening.
一看就知道他們做過什麼事
Bronchoscopy
Massive hemoptysis
Left, A: prominent areas of tissue enhancement are seen to be consistent with
intense inflammation and hypervascularity (arrows)
Swanson, K. L. et al. Chest 2002;121:789-795
Massive hemoptysis
還沒結束, 別走啊!
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
The best way to manage
the fatal asthma
The best strategy for management of acute
exacerbations of asthma is early recognition
and intervention, before attacks become
severe and potentially life-threatening.
Detailed study into the circumstances
surrounding fatal asthma have frequently
revealed failures on the part of both patients
and physicians to recognize the severity of
the disease and to intensify treatment
appropriately .
Peak flow measurement for
assessment of attack severity
Measurement of the severity of airflow
obstruction with a peak flow meter in the
home and in the medical office helps to
avoid such mistakes.
A fall to less than 50 percent of baseline
should be considered a severe attack.
A peak flow rate below 200 L/min indicates
severe obstruction for all but unusually
small adults .
Other assessment method: S / S
ARF in asthma
In the asthmatic patient with a severe acute
attack (status asthmaticus), intensive
medical therapy is usually sufficient to
improve the symptoms.
However, therapy is not invariably effective
in time to avert respiratory failure. It is
critically important to recognize
deterioration promptly, as respiratory failure
can develop very rapidly.
This may occur in part because of the
narcotizing effect of hypercapnia on
patients already fatigued from the enormous
increase in the work of breathing.
Preventing intubation
Intubation and MV may be associated
with significant morbidity and mortality,
it is desirable to avoid intubation
whenever possible.
Pharmacotherapy.
Heliox therapy; NPPV therapy: buy time
for medical therapy to work.
Indications and principles
of intubation
The decision to proceed is best based on an
integrative clinical assessment of the patient's
ability to continue ventilation until therapy
becomes effective. Worsening fatigue and
persistent or increasing hypercapnia weigh
heavily in favor of intubation.
Asthmatics have exaggerated bronchial
responsiveness, and inutbation is difficult in
any circumstance, particularly under the
conditions of hypoxia, hypercapnia, and
acidosis of respiratory failure.
The decision to proceed to intubation ＆MV
should be made before respiratory arrest.
Indications for intubation and MV
in status asthmaticus
Respiratory or cardiac arrest: must be avoided.
General appearance of the patient: change in
mental status, posture, speech, diaphoresis, extent
of accessory muscle use, RR….(most important)
(patients deteriorating on these grounds )
Increasing pulsus paradoxus
Decreasing pulsus paradoxus (exhausted pt)
Acute barotrauma
Severe lactic acidosis (esp in infants)
Silent chest despite respiratory effort
Refractory hypoxemia ( PaO2＜60 mmHg on maximal O2)
＊considered the other s/s.
Increasing PaCO2 (50mmHg＆rising＞5mmHg/hr) ＊
considered the other s/s.
The principles of intubation
To achieve prompt, complete
sedation, often by infusion of
repeated doses of one to two mg of
midazolam at two minute intervals.
To use a large endotracheal tube to
minimize added resistive load and to
facilitate suctioning of secretions.
To be prepared to infuse large
volumes of crystalloid should
hypotension result from the abrupt
shift in intrathoracic pressures.
Sedation and paralysis
Even after sedation and intubation, some patients
are unable to breathe in synchrony with the
ventilator, especially when it is set to avoid high
peak inspiratory pressures .
Paralytic agents may be necessary in this setting.
Both vecuronium and atracurium are safe and
effective in the short term. Use them just after
ensuring adequate sedation .
If used over several days, paralytic agents may
contribute to the development of an acute, diffuse
myopathy. The resulting muscle weakness can be
profound, and recovery may require many months
of rehabilitation and even then may be incomplete.
Postintubation hypotension
Incidence: 30%
Reasons:
1. Loss of vascular tone and sympathetic
activity due to sedation.
2. Hypovolemia.
3. Over Ambu bag ventilation result in severe
dynamic hyperinflation (DHI)
Severe DHI occurs, the pt becomes difficult
to ventilate, breath sounds diminish, BP falls,
and HR rises.
A trial of hypopnea or apnea is diagnostic
and therapeutic for DHI-induced hypotension.
Mechanical ventilation (MV)
Until recently, barotrauma was a common
complication of the high pressures
required to maintain normal alveolar
ventilation in patients with asthma.
Surveys of outcomes in patients requiring
mechanical ventilation prior to 1990
showed mortality rates as high as 38
percent, with many deaths resulting from
pneumothorax and ventilator malfunction .
The history of MV in
obstructive airways disease
Conventional MV for acute asthma has been
associated with a mortality in excess of 20 %, owing
to a significant incidence of barotrauma .
A strategy of permissive hypercapnia ventilation
(PHV) was first reported in 1983. No deaths were
reported in 26 asthmatics who received MV at tidal
volumes of 8 to 12 mL/kg and low respiratory rates (6
to 10 /min; peak inspiratory pressures were kept
under 50 cmH2O.
To maintain a low peak airway pressure, respiratory
drive was suppressed as needed with diazepam
and/or pancuronium, and inspiratory flow rates were
at times decreased.
Recent change in
ventilator strategy
Recent sharp reduction in mortality in this setting
was the realization that, as long as arterial
oxygenation is adequate, the risks of hypercapnia
are far smaller than the risks of excessively high
inspiratory pressures .
The key element to this approach, referred to as
permissive hypercapnia ventilation (PHV), is to
set the ventilator to deliver tidal volumes small
enough and at a frequency slow enough to keep
plateau pressure under 30 cmH2O.
This regimen is continued as long as necessary
providing oxygenation can be maintained and the
PaCO2 does not rise above 90 mmHg.
Measuring dynamic hyperinflation
A measure of lung hyperinflation has been used to
regulate levels of MV.
This measurement consists of collecting all the
exhaled gas from paralyzed, ventilated patients after
40 to 60 seconds of apnea. This volume is termed
"end-inspiratory lung volume above FRC" (VEI).
Most barotrauma and hypotension
complications of ventilation are avoided when VEI
is maintained below 20 mL/kg. The ventilator
settings are adjusted to achieve this goal, mostly by
keeping minute ventilation below 115 mL/kg/min.
Another approach to monitoring and minimizing
hyperinflation by keeping Pplat ＜ 30 cmH2O can
decrease complications.(check Pplat with a single
breath only)
Mechanical ventilation: initial settings
Mode : pharmacologically controlled; A/C; or SIMV.
FiO2 : 1.0 or sufficient to keep PaO2 ≧ 60 mmHg.
Tidal volume : 8 mL/kg ＆ Pplateau ＜30 cmH2O.
Respiratory rate : ≦ 8 /min; allow permissive
hypercapnia (PH＞7.1～7.2)
Ti : ≦1 s, keep short to avoid auto-PEEP.
I:E ratio : 1:3 to 1:5.
Inspiratory flow rates : ≧ 60 L/min.
Inspiratory wave form : decelerating/ square wave.
PEEP: increase to 80% of auto-PEEP with caution
during spontaneous breathing. (in controlled mode?)
Volume/ pressure target : Pressure or volume.
General approach to
obstructive airways disease
In general, we adhere to the low tidal volume,
low minute ventilation approach outlined
above and strive to maintain plateau airway
pressures below 30 cmH2O, irrespective of
the level of hypercapnia encountered.
(adequate sedation).
The use of PHV for obstructive airways
disease should target minimizing pulmonary
hyperinflation, not avoiding an arbitrary level
of peak airway pressure. Slow inspiratory
flows are best avoided, irrespective of their
effect on peak airway pressure.
Monitoring for asthma pt with MV
Plateau airway pressure ≦ 30 cmH2O.
Peak airway pressure ≦ 45 cmH2O.
Mean airway pressure ≦ 25 cmH2O.
Auto-PEEP.
Presence of barotrauma.
Pulse oximetry ＆ arterial blood gases.
Heart rate and blood pressure.
WEANING FROM VENTILATORY SUPPORT
It is of utmost importance to discontinue
ventilator support as soon as possible.
Intubation itself provides an ongoing irritant
stimulus and can cause bronchoconstriction.
Do not wean the asthmatic pt; discontinue
ventilatory support when the volumes ＆
pressures have markedly improved, and
clinically pt is alert, oriented, and cooperative.
Most pt can discontinue the ventilator within
48 hours.
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溺水(Near drowning)
煙霧吸入嗆傷(Smoke inhalation)
一氧化碳中毒(CO intoxication)
張力性氣胸(Tension pneumothorax)
大咳血(Massive hemoptysis)
氣喘(Asthma)
急性呼吸窘迫症候群(ARDS)
我不行了！
THANK FOR YOUR ATTENTION