The Correlation Between Gastroesophageal Reflux Disease and

Dyspnea

Olga Ayu Pratami

030.07.198

FACULTY OF MEDICINE TRISAKTI UNIVERSITY

JAKARTA
2012
0

PREFACE
Assalamualaikum wr. wb.

In the name of Allah SWT, I want to say thanks to God, because only with God help I
can finished my paper which have a title The Correlation Between Gastroesophageal Reflux
Disease and Dyspnea on time.

This paper made in order to completed the assignment for English 3 in Faculty of
Medicine Trisakti University. I hope this paper can give us benefits and help us gaining new
information and give us the curiosity to study a new things and apply it in our life as a doctor.

In this case I also would like to thanks to Allah SWT, my parents who support me
until now, dr. Oktavianus Ch. Salim, MS. who is mentoring really helped in the process of
making this paper and all my friends who helped me to find the references and gave me
support so that I can finish the paper.

Finally, I realize that this paper is far from perfect. Critics and suggestions for this
paper are needed so that in the future, author can make paper better.

Wassalamualaikum wr. wb.

Jakarta, 2012
Olga Ayu Pratami
030.07.198
CONTENT
1

PREFACE.............................................................................................................................. 1
CONTENT............................................................................................................................. 2
ABSTRACT........................................................................................................................... 3
CHAPTER I : INTRODUCTION

Background..................................................................................................... 4
Method of collecting data................................................................................. 4
Method of writing............................................................................................ 4

CHAPTER II : GERD
Epidemiologi................................................................................................... 5
Etiology.......................................................................................................... 6
Pathophysiologi............................................................................................... 6
Diagnosis........................................................................................................ 8
Treatment......................................................................................................... 10
Prognosis........................................................................................................ 12
CHAPTER III : DYSPNEA

Epidemiologi................................................................................................. 13

Pathophysiologi............................................................................................. 13

CHAPTER IV : Association between Gastroesophageal Reflux Disease and

Dyspnea............................................................................................................. 16
CHAPTER V : CONCLUSION.............................................................................. 17
REFERENCES....................................................................................................... 18

ABSTRACT
Gastroesophageal-reflux disease (GERD) is probably the most common cause of nonpulmonary dyspnea in clinical practice. Most patients with GERD induced dyspnea have
other related symptoms (e.g. retrosternal burning, sour eructations, water brash, or
2

regurgitation) when questioned closely, but about 10% may have only dyspnea as there
presenting complaint. Patients with unexplained dyspnea should be considered to have a
pulmonary cause for their pain until proven otherwise. Patients with typical GERD symptoms
should be evaluated by an upper GI endoscopy, while in others, tests like 24-hour pH
monitoring or esophageal manometry can confirm the esophageal origin of the dyspnea.
When reflux is suspected as the cause, a therapeutic trial of proton pump inhibitors is
appropriate. Antireflux surgery is indicated only if acid reflux is proved beyond doubt and is
resistant to medical therapy. Also an important part of therapy is reassurance and careful
explanation to the patient of the esophageal and not the cardiac origin of the chest pain.

CHAPTER I
INTRODUCTION

Background
3

Dyspnea and gastroesophageal reflux disease (GERD) often coexist. However, the results of
the studies investigating the prevalence of GERD among patients with dyspnea vary greatly.
Method of collecting data
In making this paper, I collected the data about GERD and dyspnea. I collected the data from
many sources, such as from the journals, and also from medical website.
Method of writing
Chapter I is the introduction, consist of background, method of collecting data and method of
writing. Chapter II is the GERD. Chapter III is the dyspnea. Chapter IV is Association
between Gastroesophageal Reflux Disease and Dyspnea. Finally, followed by conclusion in
chapter V.

CHAPTER II
GERD
Symptoms of gastroesophageal reflux disease (GERD) are common, affecting 10%
30% of the population in Western countries. Recently, the prevalence of GERD is also
increasing in a Japanese population with a high prevalence of atrophic gastritis. Respiratory
4

diseases are also common causes for consultation in primary care, but the association
between the two diseases remains unclear. Many previous studies of the association between
the two had selection bias since data were obtained in a retrospective manner. Studies
addressing the correlation between respiratory disorders and GERD symptoms in an
unselected group of persons are sparse. The incidence of chronic bronchitis, asthma, and
chronic pulmonary disease is 1.5 times more in patients with reflux esophagitis. Other studies
demonstrated a high prevalence of GERD in asthmatic patients. Thus, although there have
been many studies that showed a close association between GERD symptoms and chronic
cough, it has been unknown whether acute cough is also associated with GERD. The aim of
this study was to evaluate the relationship between GERD and respiratory symptoms in
general practice.1
Epidemiology of GERD
Western dietary habits have made GERD a common disease. Richter and associates
reported that 25-40% of Americans experience symptomatic GERD at some point.
Approximately 7-10% of Americans experience symptoms of GERD on a daily basis.
Because many individuals control symptoms with over-the-counter (OTC) medications and
without consulting a medical professional, the actual number of individuals with GERD is
probably higher. No sexual predilection exists: GERD is as common in men as in women.
However, the male-to-female incidence ratio for esophagitis is 2:1-3:1. The male-to-female
incidence ratio for Barrett esophagus is 10:1. White males are at a greater risk for Barrett
esophagus and adenocarcinoma than other populations. GERD occurs in all age groups. The
prevalence of GERD increases in people older than 40 years. 1

Etiology
Excessive retrograde movement of acid-containing gastric secretions or bile and acidcontaining secretions from the duodenum and stomach into the esophagus is the etiologic
effector of GERD. Reflux of these secretions to some degree into the esophagus is prevalent
in the United States. From a therapeutic point of view, informing patients that gastric
5

refluxate is made up not only of acid but also of duodenal contents (eg, bile, pancreatic
secretions) is important.
A functional (frequent transient LES relaxation) or mechanical (hypotensive LES)
problem of the LES is the most common cause of GERD. Transient relaxation of the LES can
be caused by foods (coffee, alcohol, chocolate, fatty meals), medications (beta-agonists,
nitrates, calcium channel blockers, anticholinergics), hormones (eg, progesterone), and
nicotine. 1
Pathophysiology of GERD
Schematically, the esophagus, lower esophageal sphincter (LES), and stomach can be
envisioned as a simple plumbing circuit as described by Stein and coworkers. The esophagus
functions as an antegrade pump, the LES as a valve, and the stomach as a reservoir. The
abnormalities that contribute to GERD can stem from any component of the system. Poor
esophageal motility decreases clearance of acidic material. A dysfunctional LES allows reflux
of large amounts of gastric juice. Delayed gastric emptying can increase volume and pressure
in the reservoir until the valve mechanism is defeated, leading to GERD. From a medical or
surgical standpoint, it is extremely important to identify which of these components is
defective so that effective therapy can be applied.1
Esophageal defense mechanisms, Esophageal defense mechanisms can be broken down
into 2 categories (ie, esophageal clearance and mucosal resistance). Proper esophageal
clearance is an extremely important factor in preventing mucosal injury. Esophageal
clearance must be able to neutralize the acid refluxed through the lower esophageal sphincter.
(Mechanical clearance is achieved with esophageal peristalsis; chemical clearance is achieved
with saliva.) Normal clearance limits the amount of time the esophagus is exposed to refluxed
acid or bile and gastric acid mixtures. Abnormal peristalsis can cause inefficient and delayed
acid clearance.1
Whether peristaltic dysfunction is secondary to esophageal exposure to acids or a
primary defect is not understood clearly. In a review by Kahrilas et al, peristaltic dysfunction
was progressively more common in patients with greater degrees of esophagitis. Abnormal
peristalsis was identified in 25% of patients with mild esophagitis and 48% of patients with
severe esophagitis.
Buttar and associates described the importance of esophageal mucosal resistance as a
protective mechanism. They classified the factors into pre-epithelial, epithelial, and
6

postepithelial defenses. When the defenses fail, esophagitis and other complications of reflux
disease arise.1
Dysfunction of the lower esophageal sphincter, The lower esophageal sphincter (LES)
is defined by manometry as a zone of elevated intraluminal pressure at the esophagogastric
junction. For proper LES function, this junction must be located in the abdomen so that the
diaphragmatic crura can assist the action of the LES, thus functioning as an extrinsic
sphincter. In addition, the LES must have a normal length and pressure and a normal number
of episodes of transient relaxation (relaxation in the absence of swallowing).2
LES dysfunction occurs via one of several mechanisms: transient relaxation of the LES
(most common mechanism), permanent LES relaxation, and transient increase of intraabdominal pressure that overcomes the LES pressure.1
Delayed gastric emptying, The postulated mechanism by which delayed gastric
emptying may cause GERD is an increase in gastric contents resulting in increased
intragastric pressure and, ultimately, increased pressure against the lower esophageal
sphincter. This pressure eventually defeats the LES and leads to reflux. However, objective
studies have produced conflicting data regarding the role of delayed gastric emptying in the
pathogenesis of GERD.1
Hiatal hernia, When discussing mechanisms for GERD, the issue of hiatal hernia must
be addressed. Hiatal hernias can be encountered frequently in patients with reflux disease;
however, it has been well proven that not all patients with hiatal hernias have symptomatic
reflux.1
Obesity as contributing factor, Some studies have shown that GERD is highly prevalent
in patients who are morbidly obese and that a high body mass index (BMI) is a risk factor for
the development of this condition. The hypothesis that obesity increases esophageal acid
exposure is supported by the documentation of a dose-response relationship between
increased BMI and increased prevalence of GERD and its complications. Therefore, the
pathophysiology of GERD in patients who are morbidly obese might differ from that of
patients who are not obese. The therapeutic implication of such a premise is that the
correction of reflux in patients who are morbidly obese might be better achieved with a
procedure that first controls obesity.
The mechanism by which a high BMI increases esophageal acid exposure is not
completely understood. Increased intragastric pressure and gastroesophageal pressure
gradient, incompetence of the lower esophageal sphincter (LES), and increased frequency of
7

transient LES relaxations may all play a role in the pathophysiology of GERD in patients
who are morbidly obese. 2
Diagnosis of GERD
When patients present with typical symptoms and no complications, the diagnosis of
GERD is usually straightforward. The classic symptoms are heartburn and regurgitation,
which may also include dysphagia.2
In the absence of classic symptoms, GERD becomes more difficult to diagnose. Other
symptoms that may be caused by GERD are atypical chest pain, hoarseness, nausea, cough,
odynophagia and asthma. Symptoms that may indicate a more serious problem, such as chest
pain (possible cardiac causes), dysphagia, odynophagia and weight loss (possible esophageal
stricture or cancer), require more extensive investigation before the diagnosis of GERD can
be established. Diagnostic tests are used when the diagnosis is in doubt or complications are a
concern.2
Response to Omeprazole, a recent study demonstrated a potential role for a proton
pump inhibitor, omeprazole (Prilosec), in the diagnosis of GERD. The response of symptoms
to omeprazole, in a dosage of 40 mg per day for 14 days, was shown to be about as specific
and sensitive for the diagnosis of GERD as the results of 24-hour pH monitoring. Because of
the efficacy of omeprazole in relieving reflux symptoms, failure to respond to this proton
pump inhibitor warrants investigation of other possible causes for a patient's symptoms.2
Radiologic finding, only one third of patients with GERD have radiologic signs of
esophagitis. Findings include erosions and ulcerations, strictures, hiatal hernia, thickening of
mucosal folds and poor distensibility. Only a minority of patients with documented abnormal
pH have radiographically evident esophagitis. Consequently, a radiographic study is not the
test of choice for the diagnosis of GERD.2
Endoscopy is useful for diagnosing the complications of GERD, such as Barrett's
esophagus, esophagitis and strictures, but it is not sensitive for diagnosis of GERD itself.
Only 50 percent of patients with GERD manifest macroscopic evidence on endoscopy.2
Ambulatory pH monitoring is generally considered the diagnostic gold standard for use
in patients with GERD. In this study, a pH monitor is placed in the esophagus above the
lower esophageal sphincter, and the pH is recorded at given moments in time. Over the 24hour test period, the patient writes down the time and situation in which symptoms occur, in

the hope that symptoms can be correlated with the lowering of esophageal pH that occurs
with reflux.3
Esophageal pH monitoring may not be available in some areas. Furthermore, the test is
time-consuming, and it can be inconvenient or troublesome for the patient. In addition, pH
monitoring requires good technical placement of the probe and experienced interpretation of
the results.3

Treatment of GERD
Avoiding foods and beverages that can weaken the LES is recommended. These foods
include chocolate, peppermint, fatty foods, coffee, and alcoholic beverages. Foods and
beverages that can irritate a damaged esophageal lining, such as citrus fruits and juices,
tomato products, and pepper, should also be avoided. 1,2
Decreasing the size of portions at mealtime may also help control symptoms. Eating
meals at least 2 to 3 hours before bedtime may lessen reflux by allowing the acid in the
stomach to decrease and the stomach to empty partially. In addition, being overweight often
worsens symptoms. Many overweight people find relief when they lose weight.
Cigarette smoking weakens the LES. Therefore, stopping smoking is important to reduce
GERD symptoms.
Elevating the head of the bed on 6-inch blocks or sleeping on a specially designed
wedge reduces heartburn by allowing gravity to minimize reflux of stomach contents into the
esophagus. 2
Antacids taken regularly can neutralize acid in the esophagus and stomach and stop
heartburn. Many people find that nonprescription antacids provide temporary or partial relief.
An antacid combined with a foaming agent such as alginic acid helps some people. These
compounds are believed to form a foam barrier on top of the stomach that prevents acid
reflux from occuring.
Long-term use of antacids, however, can result in side effects, including diarrhea,
altered calcium metabolism (a change in the way the body breaks down and uses calcium),

and buildup of magnesium in the body. Too much magnesium can be serious for patients with
kidney disease. If antacids are needed for more than 3 weeks, a doctor should be consulted. 2
For chronic reflux and heartburn, the doctor may prescribe medications to reduce acid in the
stomach. These medicines include H2 blockers, which inhibit acid secretion in the stomach.
Currently, four H2 blockers are available: cimetidine, famotidine, nizatidine, and ranitidine.
Another type of drug, the proton pump (or acid pump) inhibitor omeprazole inhibits an
enzyme (a protein in the acid-producing cells of the stomach) necessary for acid secretion.
The acid pump inhibitor lansoprazole is currently under investigation as a new treatment for
GERD.
Other approaches to therapy will increase the strength of the LES and quicken
emptying of stomach contents with motility drugs that act on the upper gastrointestinal (GI)
tract. These drugs include bethanechol and metoclopramide.
Tips To Control Heartburn
1. Avoid foods and beverages that affect LES pressure or irritate the esophagus lining,
including fried and fatty foods, peppermint, chocolate, alcohol, coffee, citrus fruit and
juices, and tomato products.
2. Lose weight if overweight.
3. Stop smoking.
4. Elevate the head of the bed 6 inches.
5. Avoid lying down 2 to 3 hours after eating.
6. Take an antacid.
People with severe, chronic esophageal reflux or with symptoms not relieved by the treatment
described above may need more complete diagnostic evaluation. Doctors use a variety of
tests and procedures to examine a patient with chronic heartburn.
An upper GI series may be performed during the early phase of testing. This test is a
special x-ray that shows the esophagus, stomach, and duodenum (the upper part of the small
intestine). While an upper GI series provides limited information about possible reflux, it is
used to rule out other diagnoses, such as peptic ulcers.
Endoscopy is an important procedure for individuals with chronic GERD. By placing a
small lighted tube with a tiny video camera on the end (endoscope) into the esophagus, the
10

doctor may see inflammation or irritation of the tissue lining the esophagus (esophagitis). If
the findings of the endoscopy are abnormal or questionable, biopsy (removing a small sample
of tissue) from the lining of the esophagus may be helpful.
The Bernstein test (dripping a mild acid through a tube placed in the mid-esophagus) is
often performed as part of a complete evaluation. This test attempts to confirm that the
symptoms result from acid in the esophagus. Esophageal manometric studies-pressure
measurements of the esophagus-occasionally help identify critically low pressure in the LES
or abnormalities in esophageal muscle contraction. 1
For patients in whom diagnosis is difficult, doctors may measure the acid levels inside
the esophagus through pH testing. Testing pH monitors the acidity level of the esophagus and
symptoms during meals, activity, and sleep. Newer techniques of long-term pH monitoring
are improving diagnostic capability in this area.3
Prognosis
Most patients with GERD do well with medications, although a relapse after cessation
of medical therapy is common and indicates the need for long-term maintenance therapy.
Identifying the subgroup of patients who may develop the most serious complications
of GERD and treating them aggressively is important. Surgery at an early stage is most likely
indicated in these patients. After a laparoscopic Nissen fundoplication, symptoms resolve in
approximately 92% of patients.
Most cases of gastroesophageal reflux in infants and very young children are benign
and respond to conservative nonpharmacologic treatment (developmental disabilities
represent an important diagnostic exception); 80% resolve by age 18 months (55% resolve by
age 10 mo). Some patients require a "step-up" to acid-reducing medications, and only a very
small minority require surgery. Because symptomatic gastroesophageal reflux after age 18
months likely represents a chronic condition, long-term risks are increased. For patients
whose gastroesophageal reflux persists into later childhood, long-term therapy with
antisecretory agents is often required.

11

In refractory cases or when complications related to reflux disease are identified (eg,
stricture, aspiration, airway disease, Barrett esophagus), surgical treatment (fundoplication) is
typically necessary. The prognosis with surgery is considered excellent. The surgical
morbidity and mortality is higher in patients who have complex medical problems in addition
to gastroesophageal reflux. 1

CHAPTER III
DYSPNEA
Dyspnea, can be defined as an uncomfortable awareness of breathing. Dyspnea has
been classified as acute or chronic on the basis of the tempo. Acute dyspnea is defined as
dyspnea arising in the previous 24 to 48 hours. It is a frequent, badly tolerated symptom, but
not a sign. It is a subjective sensation, with various intensities, for which there is no accurate
objective measurement.2 The patients do not use the word itself so that the physician has to
interpret the patients symptoms and decide what is dyspnea and what not.6
Epidemiology of Dyspnea
Dyspnea is a common chief complaint among patients who come to the emergency
department (ED). A chief complaint of dyspnea or shortness of breath made up 3.5 percent of
the more than 115 million visits to United States EDs in 2003. Other dyspnea-related chief
complaints (cough, chest discomfort) comprised 7.6 percent.
According to one prospective observational study, the most common diagnoses among
elderly patients presenting to an ED with a complaint of acute shortness of breath and
manifesting signs of respiratory distress (eg, respiratory rate >25, SpO2 <93 percent) are
decompensated heart failure, pneumonia, chronic obstructive pulmonary disease, pulmonary
embolism, and asthma.4
Pathophysiology of Dyspnea5

Production of Dyspnea
Dyspnea develops when there is a
Primary Causes

mismatch between central respiratory

motor activity and incoming afferent
information from receptors in the
12

airways, lungs and chest wall structures.

Dyspnea occurs when ventilatory demand

cannot be met by the body's ability to
respond.

The perception of respiratory effort

increases whenever the central motor
command to the respiratory muscles must
be increased; i.e. increase mechanical
load or weakened muscles and the
increased work of breathing.
CHF

The sense of air hunger, as

described in patients with
congestive heart failure, has
been shown to be associated
with increases in ventilatory
drive, particularly in the
presence of hypoxemia or

Bronchial Asthma

hypercapnia.
The sensation of chest tightness is
associated with
bronchoconstriction. It
develops early in the
process with mild airway
obstruction. With
progressive decline in the
lung function, increased
respiratory effort follows
and lastly, air hunger
13

develops.
Perception of Dyspnea
Temporary dyspnea in
healthy persons

Healthy persons may perceive dyspnea

due to exercise, but it is short lived and
well tolerated.

Chronic dyspnea
secondary to illness

Dyspnea occurs in patients with chronic

disease when ventilatory demands exceed
supply. It is multifactorial.

Mood, Stress and Fatigue

Fatigue and mood changes such as anxiety,

depression, somatization, and hostility
significantly increase with high intensity of
dyspnea in asthma.
In an epidemiologic study of healthy
individuals, increase in anxiety, anger,
depression associated with increase of
respiratory symptoms including dyspnea.
Anxiety has been shown to significantly
correlate with the intensity of dyspnea, as in
cancer patients.

Personality

Personality influences perception of

dyspnea:

in emphysema, nervousness and

cyclic tendency are the determinants
for dyspnea, in addition to anxiety

in asthma, the severity of disease is

linked to psychological disturbances
and poor perception of
breathlessness, and

in hypochondriacs dyspnea is related

to severity.

14

CHAPTER IV

Association between Gastroesophageal Reflux Disease and Dyspnea

Sufferers describe dyspnea as a horrible feeling of shortness of breath, a sensation of
increased effort or tiredness in moving the chest muscles, a feeling of being smothered, or a
sense of cramping or tightening of the chest wall. Add to this a searing pain in the chest, a
hallmark of GERD, and your cup of woes is brimming over.
There are various causes for shortness of breath such as hyperthyroidism,
hypothyroidism, chronic anxiety disorders, deformities of the chest or obesity which can limit
the movement of the chest wall and the decrease the ability of the lungs to fill completely.
GERD or gastroesophageal reflux disease may also be a cause of dyspnea.
GERD is the backward flow of stomach acids into the esophagus. Generally, the
contents of the stomach and stomach acid are prevented from backing up or refluxing into the
esophagus by a valve at the bottom of the esophagus known as the lower esophageal
sphincter. When this valve misfunctions, acid enters the lower part of the esophagus, resulting
in the rather familiar burning sensation referred to as heartburn. If left untreated, GERD can
ultimately lead to lung damage, ulcers in the esophagus and esophageal cancer.
To isolate shortness of breath resulting from GERD, the patients history which records
necessary information such as history gastroesophageal reflux disease, asthma, or other
allergic conditions, the presence of chest pain, recent accidents or surgeries, information
regarding smoking habits, level of physical activity and exercise habits and any psychiatric
history would be useful to the physician.
Once the cause of dyspnea it can be treated accordingly. If GERD is the cause then it
can be managed with antacids, other medications and dietary changes.1
However effective over-the-counter medicines may be self medication is not the key. Getting
an accurate diagnosis and treating the root cause is a better way of preventing the problem
from escalating. 2

CHAPTER V
15

CONCLUSION
There are various causes for shortness of breath such as hyperthyroidism,
hypothyroidism, chronic anxiety disorders, deformities of the chest or obesity which can limit
the movement of the chest wall and the decrease the ability of the lungs to fill completely.
GERD or gastroesophageal reflux disease may also be a cause of dyspnea.

REFERENCES

16

1. Patti MG. Gastroesophageal Reflux Disease. August 19, 2011 [cited 2012 januari].
Available: http://emedicine.medscape.com/article/176595-overview#a0104
2. Scott M, Gelhot AR. Gastroesophageal Reflux Disease: Diagnosis and Management. Am
Fam Physician. 2002; 59(5):1161-9.
3. Sarani B, Gleiber M, Evans SR. Esophageal pH monitoring, indications, and methods. J
Clin Gastroenterol 2002; 34(3):200-6.
4. Zaw K, Periyakoil VS. Dyspnea: How to Assess and Palliate Dyspnea. November 16, 2006
[cited 2012 january].
Available: http://summit.stanford.edu/pcn/M07_Dyspnea/pathophys.html
5. Boyars MC, Karnath BM, Mercado AC. Acute dyspnea: A sign of underlying disease.
Hosp Phys 2004;7:23-7.

17