JUNE 17, 2014

RESPIRATORY SYSTEM

CHAPTER 33: DYSPNEA

Dyspneasubjective
experience
of
breathing
discomfort that consists of quality distinct sensations
that vary in intensity.
-must be distinguished from the signs of increased
work of breathing.
-more commonly viewed as holistic than pain
sensations which are attributed to the stimulation of a
single nerve ending only

-Baseline Dyspnea Index and Chronic Respiratory

Disease Questionnaire- to gain sense of patients
disability
Affective dimension- air hunger evokes stronger
affective response than does inc effirt of work of
breathing. Affective dimension can be altered to treat
dyspnea
DIFFERENTIAL DIAGNOSIS

MECHANISMS OF DYSPNEA
Motor Efferent- outgoing motor output from the brain
to the ventilatory muscles (feed forward)
-disorders of the ventilator pump (inc. airway
resistance or stiffness/decreased compliance) are
assoc. with inc. work of breathing or a sense of
increased effort to breath.
Sensory Afferent- incoming sensory input from the
receptors throughout the body (feedback)
-hypoxemia,
acute
hypercapnia,
academiaall
stimulate the chemoreceptors in the carotid bodies and
medulla
---increase in ventilation producing air
hunger
-bronchospasm ---mechanoreceptors in the lung
sensation of chest tightness
-interstitial edema and pulmonary vascular receptors
activates the J receptors and leads to air hunger
-hyperinflation- assoc with the sensation of inc work of
breathing and inability to get a deep breath
-metaboreceptors in skeletal muscles aare activated by
changes in the local biochemical milieu of the tissue
active during exercise; when activated contributes to
the breathing discomfort
INTEGRATION: EFFERENT-REAFFERENT MISMATCH
-increases intensity of dyspnea. This is important when
there is mechanical derangement of ventilator pump
such as in asthma and COPD
ANXIETY

-Acute anxiety inc severity of dyspnea bec of altered

interpretation of sensory data
-if (+) expiratory flow limitation, the inc RR that
accompanies acute anxiety leads to: HYPERINFLATION,
INC WORK OF BREATHING , SENSE OF UNSATISFYING
BREATH
ASSESSING DYSPNEA
Quality of sensation- determine quality of discomfort,
dyspnea questionnaires, phrases used by patients to
assist in describing the breathing sensations
Sensory intensity- modified Borg scale/ visual analogue
scale to measure dyspnea at rest, after exercise or
recall of a reproducible task (climbing stairs)

yEi (,)(,)

Dyspnea in Respi

Dyspnea in Cardio

Due to alteration in the

mechanical properties of
the lungs/ chest wall,
airways
or
lung
parenchyma

Due to gas exchange

abnormalities
or
stimulating
pulmonary/
vascular receptors

MECHANISMS OF DYSPNEA IN COMMON DSES

DPWH MAV- inc Drive to breath; stimulation of
Pulmonary receptors; inc Work of Breathing;
Hypoxemia; Metaboreceptors; Acute hypercapnia;
stimulation of Vascular receptors
COPD- WAH
ASTHMA- A.DPWH
ILD/ interstitial lung disease- A.DPWH
PVD/ pulmonary vascular disease- DH.V
CPE/ cardiogenic pulmonary edema- DPWH MV
NCPE/ noncardiogenic pulmo edema- DPWH
ANEMIA- M
DECONDITIONING M
RESPIRATORY SYSTEM DYSPNEA
A.

Dses of the airways

-asthma and COPD (MC obstruclive lung dses) are

charac by expiratory airflow limitation leading to
dynamic hyperinflation of the lungs and chest wall.
May lead to hypoxemia and hypercapnia from V/Q
mismatch
-moderate to severe dses- inc resistive and elastic
loads and inc work of breathing
-bronchoconstrictionchest
tightness
and
hyperventilation due to stim of pulmo receptors
B. Dses of the chest wall
-kyphoscoliosis,
Myas
syndrome
-Large pleural effusion

gravis

and

GuillainBarre

C. Dses of lung parenchyma

-Interstitial lung dses from infections, occupl
exposures, autoimmune disorders- all lead to stiffness/
dec compliance and inc work of breathing
-v/q mismatch. Destn/thickening of alveolar capillary
interface lead to hypoxemia and inc drive to breathe

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RESPIRATORY SYSTEM
PULSUS paradoxus- if >10mmHg, CPD or asthma

CARDIOVASCULAR SYSTEM DYSPNEA

A.

Dses of the left heart

-myocardial dses lead to greater left ventricular end

diastolic volume, elevation of left ventricular end
diastolic, elevated pulmo pressures
-leads to interstitial edema and stim of pulmo receptors
Diastolic dysfunction (VERY STIFF LEFT VENTRICLE)
severe dyspnea with mild degrees of activity esp if
assoc with mitral regurgitation

B. Dses of the pulmo vasculature

-pulmo thromboembolic dse , primary dse of pulmo
circulation cause dyspnea via inc pulmo artery
pressure
-hyperventilation is most common; hypoxemia may be
present
C. Dses of the pericardium

Cirrhosis- spider angiomata, gynecomastia

Dullness- pleural effusion
Hyperresonance- emphysema
Cardiac axam: focus on elevated pressures in the right
side e.g. JVD, edema, accentuated pulmonic to the
second heart sound; left ventricular dysfunction (s3
and s4 gallops) ; valvular dse(murmurs)
Inward
motion
of
abdomen
diaphragmatic weakness

on

inspiration-

Outward motion of abdomen on exhalation- pulmonary

edema
Clubbing- interstitial pulmonary fibrosis
Joint swelling and deformation, raynauds- indicative of
collagen vascular process assoc with pulmo dse

-constrictive pericarditis cardiac tamponade

Hyperinflation- obstructive lung dses
DYSPNEA WITH NORMAL RESPI AND CARDIO
SYSTEMS
Mild anemia- breathing discomfort during exercise; (+)
stimulation of metaboreceptors; oxygen saturation is
normal
Obesity- dyspnea due to high cardiac output an
impaired ventilator pump fxn
Cardiovascular deconditioning/ poor fitness- anaerobic
metabolism and stim of chemo and metaboreceptors
APPROACH TO PATIENT
Orthopnea- mc indicator of CHF

Low lung volume- interstitial edema or fibrosis,

diaphragmatic dysfxn, impaired chest wall motion
Prominent pulmo vasculature in the upper zonespulmo venous HTN
Enlarged central pulmo arteries- pulmo artery HTN
Enlarged cardiac silhouette- dilated cardiomyopathy or
valvular dse
Bilateral pleural effusion- CHF and collagen vascular
dse
Unilateral effusion- carcinoma and pulmo embolism,
heart failure

Obesity- mechanical impairment of diaphragm

Asthma- triggered by esophageal reflux
Nocturnal dyspnea- CHF or asthma
Acute, intermittent dypnea- MI, bronchospasm or
pulmo embolism

Electrocardiogram- ventricular hypertrophy and prior

MI
Echocardiography- systolic dysfxn. Pulmo HTN, valvular
heart dse
Bronchoprovocation- intermittent symptoms suggestive
of asthma but normal Pe and lung fxn

Chronic persistent dyspnea- COPD, interstitial lung dse,

chronic thromboembolic dse

DISTINGUISHING RESPI FROM CARDIO DYSPNEA

Platypnea- dyspnea in upright postion relieved by

supine position; assoc with left atrial myxoma or
hepatopulmonary syndrome

Repiratory- if at peak exercise, pt reached predicted

maximal ventilation, demonstrates increased dead
space or hypoxemia, or develops bronchospasm

Evidence for inc work of breathing- supraclavicular

retractions, use of accessory muscles and tripod
position (all suggest inc in AW resistance or stiff lungs
and chest wall)

Cardio- heart rate is >85percent of the predicted

maximum,
anaerobic
threshold
occurs
early,
excessively high BP or decreases during exercise, O2
pulse falls, ischemic changes on ECG

yEi (,)(,)

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RESPIRATORY SYSTEM

TREATMENT
First goal: correct underlying problem responsible for
the symptom
Supplemental O2- if resting O2 saturation is less than
or equal to 89percent
COPD- pulmonary rehab
cold air on face, chest wall vibration, inhaled
furosemide- under investigation

-dysfxn of surfactant , inc surface forces, propensity of

alveoli to collapse
Physiologically- NCPE is charac by intrapulmonary
shunt with hypoxemia and decreased pulmonary
compliance
Pathologically- evident alveolar hyaline membranes,
inflammation with pulmo fibrosis
COMMON CAUSES OF NCPE

PULMONARY EDEMA
Albumin- low in cirrhosis and nephritic syndrome
CARDIOGENIC PULMONARY EDEMA
-cardiac abnormalities leading to inc pulmonary venous
pressure
-early signs: exertional dyspnea and orthopnea. Chest
radiograph shows Peribronchila thickening, prominent
vascular markings In upper lung zones and Kerley B
lines.
-alveoli fill with fluid- patchy alveolar filling on
radiograph in perihilar distribution. Progresses to
diffuse alveolar infiltrates
-(+) ronchi and wheezes

a.

-Pneumonia, chest trauma(pulmo contusion),smoke

inhalation,
oxygen
toxicity,
aspiration,
pulmo
embolism(reperfusion)
b.

-Due to damage of pulmonary capillary lining with

leakage of proteins and other macromolecules into the
lungs

yEi (,)(,)

Indirect/ Hematogenous injury to the lung

MaNiLa PICS

-multiple
transfusions,
nonthoracic
trauma,
leukoagglutination rxns, pancreatitis, iv drugs e.g
heroin, cardiopulmonary bypass, sepsis
c.

NONCARDIOGENIC PULMONARY EDEMA

Direct injury to the lung PC SOAP

Possible lung injury plus elevated hydrostatic

pressure Hi RN!

-High altitude pulmo edema, Reexpansion

edema, Neurogenic pulmo edema

pulmo

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RESPIRATORY SYSTEM

Distinguishing Cardio from Noncardio Pulmo Edema

Cardiogenic

NonCardiogenic

Physical exam

Inc intracardiac pressure (S3 gallop,

elevated JVP, peripheral edema),
rales and/or wheezes

Dominated by findings of the

precipaitating conditions; pulmonary
findings maybe normal in early
stages

Chest radiograph

Enlarged cardiac silhouette, vascular

redistribution, interstitial thickening ,
perihilar alveolar infiltrates, pleural
effusions common

Heart size normal, alveolar infiltrates

more uniformly distributed, pleural
effusions no common

Hypoxemia

Due largely to v/q mismatch and

responds to supplemental O2

Due to intrapulmonary shunting,

persists despite high concentrations
of inhaled O2

Association of Qualitative Descriptors and Pathophysiologic Mechanisms of SOB

Descriptor

Pathophysiology

Chest tightness, constriction

Bronchoconstriction, interstitial edema ( asthma, MI)

Increased work of breathing

AW obstruction, Neuromuscular dse (COPD, mod to

severe asthma, myopathy, kyphoscoliosis)

Air hunger, need to breathe, urge to breathe

Inc drive to breath ( CHF, Pulmo emboli, mod to

severe aw obstruction

Cannot get a deep breath

Hyperinflation (asthma and copd) , restricted tidal

volume (pulmo fibrosis, chest wall restriction)

Hheavy breathing, rapid breathing, breathing

more

Deconditioning

When life gives you dirt, grow some flowers.

yEi (,)(,)

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