Title: Adenosine Induced Bronchospasm
1Adenosine Induced Bronchospasm
2Case report
- ??? 4129285
- ?? ??X
- ?? 169.5cm
- ?? 60 Kgw
- ?? 62 y/o
- ?? M
- ?? SURG-chest
3Lab.data 1
- WBC 10.1 K/µL
- RBC 5.06 M/µL
- HB 14.0 g/dL
- HCT 44.2
- PLT186.0 K/µL
- Alb 3.9 g/dL
- TP 6.1 g/dL
- PT, PTT WNL
4Lab. Data2
- UN12.2 mg/dL
- CRE 0.8 mg/dL
- UA 4.9 mg/dL
- Na 147.0 mmol/L
- K 4.0 mmol/L
- Cl 105.0 mmol/L
- Ca 2.34 mmol/L
- T-CHO 233.0 mg/dL
5EKG
- NORMAL SINUS RHYTHM, RATE 84 -- normal P axis,
PR, rate rhythm
6Imaging study
- CXR shows normal heart size with increased lung
markings. Mild fibrotic change is found at bil.
lung fields with emphysematous change at lower
lungs. COPD is suspected - HRCT of chest for the pulmonary bullous
disease1. multiple large bullae formation in
the RML (lower lung fields, at the anterior
aspect).2. diffuse pneumatoceles in both lung
fields due to COPD with emphysematous change.3.
nonspecific small nodes in the mediastinum.4.
bilateral renal cysts.
7- Impression
- COPD with emphysema large bullae in the RML.Â
- Surgical planning
- VATS for Wedge resection
8Induction for anesthesia
- Pre-oxygenation
- Drugs for intubation
- 37 ??
- Check position by fiberscope and fixed
- A-line
- CVP
9PSVT was noted during CVP insertion
- EKG showed PSVT when guide wire was inserted
- Adenosine was used for treatment via CVP
- 6 mg initial iv push , but in vain
- Another 12 mg iv push about 1 min later
- After bradycardia was showed for seconds,
- EKG was returned to sinus rhythm
10High pressure was alarmed by monitor!!
- Rechecked tube position
- High pressure was still noted
- EtCO2 and BS was decreased
- SpO2 was slight decreased
- Call VS, and check tube again
- High EtCO2 (around 70) was noted
- Bronchspasm was noted at RLL
11- Wheezing was heard after EtCO2 was showed
- Steroids and aminophylline were given
immediately. - Mild wheezing was noted 10mins later.
- No episode was noted during operation
- No wheezing was noted at the end of surgery
12Life Sciences. 69(11)1225-40, 2001 Aug 3
- Bronchospasm induced by adenosine is blocked by
representatives of all the major classes of drugs
used in the treatment of asthma. - Clinical studies have suggested involvement of
neural pathways, mast-like cells and mediators
such as histamine, serotonin and lipoxygenase
products. There is a strong link between
responsiveness to adenosine and eosinophilia. - In different animal models A1, A2b and A3
adenosine receptor subclasses have all been
implicated in inducing bronchospasm. - At least two different mechanisms, both involving
neural pathways, exist. One, involving the
adenosine A1 receptor, functions in mast cell
depleted animals the other requires interaction
with a population of mast-like cells activated
over A2b or A3 receptors.
13Life Sciences. 69(11)1225-40, 2001 Aug 3
- Not only histamine but also serotonin and
lipoxygenase products released from the mast-like
cells are potential mediators. - As mast cells both release adenosine and respond
to adenosine, adenosine provides a non-specific
method of amplifying specific signals resulting
from IgE/antigen interaction. - This mechanism may not only have a pathological
significance in asthma it may be part of a
normal bodily defense response that in asthmatic
subjects is inappropriately activated.
14Is the dyspnea during adenosine cardiac stress
test caused by bronchospasm? American Heart
Journal. 142(1)142-5, 2001 Jul.
- Adenosine cardiac stress is widely used as an
alternative to exercise testing during myocardial
perfusion imaging (MPI). Dyspnea often
accompanies the adenosine stress test. - Although known asthmatic patients are excluded
from this test because of the danger of
bronchospasm, there is incomplete information
regarding the role of factors such as chronic
obstructive pulmonary disease (COPD) and tobacco
smoking in adenosine-induced dyspnea.
15American Heart Journal. 142(1)142-5, 2001 Jul.
- PATIENTS AND METHODS
- A total of 122 consecutive patients (75 male,
47 female mean age 59 years, SD 10 years)
undergoing pharmacologic stress testing with an
intravenous infusion of adenosine also had
volume-flow spirometry (Vitalograph Compact,
Vitalograph Ltd) before, during, and after the
test. The indices assessed were forced expiratory
volume in one second, its ratio to the forced
vital capacity, and peak expiratory flow rate.
16American Heart Journal. 142(1)142-5, 2001 Jul.
- RESULTS
- Mild to severe symptoms were experienced by
81 of patients during adenosine infusion. More
than half the patients had dyspnea, but there was
no associated bronchospasm. Although the patients
with COPD showed parameters indicative of
bronchial resistance compared with those without
this problem, there was no further deterioration
after adenosine infusion. Similarly, patients
with a history of tobacco abuse, despite showing
a tendency toward increasing airways resistance,
had no bronchospasm during the administration of
adenosine.
17American Heart Journal. 142(1)142-5, 2001 Jul.
- CONCLUSIONS
- Although dyspnea is a common problem during
adenosine stress MPI, it is not associated with
any appreciable bronchospasm. - COPD and tobacco abuse do not appear to be
contraindications to adenosine stress MPI
studies. However, it is probably safe to exclude
patients with severe COPD from adenosine stress
MPI until after further evaluation with larger
numbers of patients.
18Pulmonary function monitoring during adenosine
myocardial perfusion scintigraphy in patients
with chronic obstructive pulmonary disease.
- CONCLUSION
- This study shows that adenosine can be safely
administered intravenously to selected patients
with known or suspected COPD to produce coronary
vasodilatation for myocardial perfusion imaging.
Patients who are within the guidelines
established for this study should be considered
for adenosine coronary vasodilatation with use of
bronchodilator pretreatment, a graduated dose of
adenosine, and regular chest auscultation during
the infusion. Mayo Clinic Proceedings.
74(4)339-46, 1999 Apr.
19- Prednisolone hastens recovery from
histamine-induced bronchospasm in asthmatics. - Journal of Asthma. 37(5)435-40, 2000 Aug.
20Thank you for your attention!!