pa tho physiology of dyspnea & its treatment-20090320

8/14/2019 Pa Tho Physiology of Dyspnea & Its Treatment-20090320

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2009 Mar 20

Pathophysiology ofDyspnea &

Its Treatment

PathophysiologyPathophysiology ofof

DyspneaDyspnea &&

Its TreatmentIts Treatment


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Regulation of RespirationRegulation of RespirationRegulation of Respiration

Nervous system

adjusts the rate of alveolar ventilation almostexactly to the demands of the body

PaO2 & PaCO2 are hardly to altered,even during heavy exercise & most othertypes of respiratory stress


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DRG most: located within the solitary nucleus (SN)

additional: adjacent reticular substance (RS)

SN: the sensory termination of both vagal &glossopharyngeal n. (which transmit sensorysignals into the RC from chemoreceptors,

baroreceptors, several types of receptors inthe lungs) control inspiration!! control Resp Rhythm!!


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PTC (pneumotaxic center)

located dorsally in the nucleus parabrachialisof the dorsosuperior pons

primary effect: basic oscillatory mechanism tocontrol the switch-off point of the inspiratoryramp

to limit inspiration!! to increase Resp Rate!! controlling the duration of the filling phase of the

lung cycle

signal strong: inspiration 0.5 secsignal weak: inspiration 5 sec


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Regulation of RespirationRegulation of RespirationRegulation of Respiration VRG

found in the nucleus ambiguus & nucleusretroambiguus

remain almost totally inactive during normal-quietrespiration

no evidence of participating in the basic rhythmicaloscillation that controls resp

contributes extra inspiratory drive, if high insp drive

spill over from DRG provide powerful expiratory signals to abdominal m.

during very heavy expiration overdrive

mechanism!! (esp during heavy exercise)


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Chemical Control of RespirationChemical Control of RespirationChemical Control of Respiration Peripheral chemoreceptor

system

chemoreceptors in severalareas outside the brain

important for detecting changesin PaO2

also respond to a lesser extentto changes in CO2 & [H+]

transmit nervous signals to theRC in the brain

carotid bodies, aortic bodies,other a. of thoracic &

abdominal regions


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Chemical Control of RespirationChemical Control of RespirationChemical Control of Respiration Low PaO2 stimulate

alveolar ventilation

when PCO2 & [H+] kept

constant at normal levels

almost no effect onventilation as long as

PaO2 remains >100mmHg ventilation doubles

when PaO2 falls to60mmHg


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Other Factors Affecting RespirationOther Factors Affecting RespirationOther Factors Affecting Respiration

Volutary control for short periods of time, one can hyper- or hypo-

vent to serious derangements in PCO2, pH, PO2

Irritant receptor in the airways

stimulated by many incidents causing cough,

sneeze, bronchoconstriction J receptor in alveolar wall, juxtaposition to pulmonary capillaries

stimulated when pc engorged with blood, when

pul edema occurs causing dyspnea


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Other Factors Affecting RespirationOther Factors Affecting RespirationOther Factors Affecting Respiration

Brain edema activity of RC depressed or inactivated

damaged brain tissue swell, compressing the cerebral a.,partially blocking cerebral blood supply

hypertonic solution: remove fluids in brain,ICP, re-establishing respiration within mins

Anesthesiapentobarbital: depress RC strongest

morphine: only as an adjunct to anesthetics, becausegreatly depress RC, while lessly anesthetize cerebral

cortex


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O2 or CO2 for control of RC?O2 or CO2 for control of RC?O2 or CO2 for control of RC? changes in PO2:

no direct effect on RC itself to alter resp drive only indirect effect acting through peripheral

chemoreceptors

Hb-O2 buffer system delivers almost exactly normal

amounts of O2 even when PO2 changes from 60 to1000mmHg

adequate DO2, despite changes in pulmonary ventilation

changes in PCO2: both blood & tissue PCO2 changes inversely with therate of pulmonary ventilation

animal evolution CO2: THE MAJOR CONTROLLER

OF RESPIRATION


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Dyspnea = SOB Air HungerDyspneaDyspnea = SOB= SOB Air HungerAir Hunger Definition: subjective mental anguish

associated with inability to ventilate enoughto satisfy the demand for air causingexperience of breathing discomfort

Sensation of dyspnea have 2 components: Urge to breathe = air hunger

Excessive effort sensation = perception of

sensation Can be separated experimentally

in voluntarily hyperventilating normal subjects,

addition of CO2 results in sense of urge to breatheBUT awareness of effort of breathing


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Dyspnea = SOB Air HungerDyspneaDyspnea = SOB= SOB Air HungerAir Hunger Urge to breath

Sensory input to the cerebral cortex: consists ofinformation form mechanoreceptors

Resp apparatus (predominantly the upper airways)

& face BUT, no specific area in CNS identified as

sensory locus for dyspnea

Excessive effort sensation Interpretation of information arriving at

sensorimotor cortex

Depends on psychological makeup of the person


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Dyspnea = SOB Air HungerDyspneaDyspnea = SOB= SOB Air HungerAir Hunger A range of sensation:

from awareness of breathing to resp distress The wide range of meanings on several

counts:

Subjective complaint w/o consistency in objective signs(eg tachypnea)

Few physicians have experienced the resp discomforta/w chest dz (extrapolations from normal breathlessness,

eg after strenuous exercise) Most experimental observations based on the study of

normal subjects or animals under artificial circumstances

Apply the term loosely, based on the predominant ptpopulation the physicians served


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Dyspnea = SOB Air HungerDyspneaDyspnea = SOB= SOB Air HungerAir Hunger

Results from some pathophysiologic event influenced by psychological state, bodily

preoccupation, level of awareness, usual

level of physical activity, body weight, stateof nutrition, medications

Many modifying factors variablecorrelation between dyspnea ratingsairflowlimitationexercise performance


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Dyspnea = SOB Air HungerDyspneaDyspnea = SOB= SOB Air HungerAir Hunger Three factors: development of this sensation

Abnormality of resp gases in the body fluid, esphypercapnia (a much less extent, hypoxia) excess buildup of CO2 in the body fluid, a person becomes verydyspneic

Amount of work performed by the resp m. toprovide adequate ventilation at times, CO2 & O2 level in body fluids are normal, but to attain

this normality of resp gases, the person has to breathe forcefullyState of mind persons resp functions is normal & still dyspnea: neurogenic oremotional dyspnea, eg, psychological fear of not being able to

receive a sufficient quantity of air on entering small or crowed rooms


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea

Activation of resp complex efferent command to breathe to lungs & CW

Voluntary output from 1 motor cortex ventilation coactivation of 1sensory cortex

Input from lung & CW 1 sensory cortex affect the perception

Emotions, cognition, personality affect central experience of dyspnea

efferent

afferent


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea As with all sensations, result from changes

in neural activity within the cortical structuresthat are responsible for sensory perception

Unlike localized sensations(eg touch,

temperature, arise from peripheral receptor stimulation),

dyspnea is a vague visceral sensation

(analogous to thirst or hunger), more dependenton neural activity arising from within CNS;

exercise, breath-holding, anemia causing dyspnea do not have a

common pattern of peripheral receptor stimulation


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea Imaging of brain function (PET, fMRI)

Dyspnea perception neural activity activation oflimbic & paralimbic structures (phylogenically ancient regions ofcerebral cortex) also seen in brain imaging studies of pain,thirst, hunger

So dyspnea is a primal experience associated withbehaviors intended to counteract a threat to survival

Interestingly, increasing resp effort + mild insp loadinsufficient to provoke urge to breath activation ofsensory cortex & not limbic structure

Good evidence: dyspnea sensation depends on, to alarge extent, the degree to which resp-related neurons in

the brainstem are stimulated


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea Dyspnea with lung disease

Increased central resp drive necessary toachieve adequate ventilation by a mechanicallycontrained resp apparatus

eg, COPD progressive hyperinflation /c increasing dyspnea,as ventilatory demands require greater resp m. activity 1. toovercome increased elastic work at high lung volume 2. to offsetforeshortening of insp m. that places them at a mechanical

disadvantage

LVRS successful lessening of dyspnea, consistent withimprovement in both lung & resp m. mechanics alleviation ofhyperinflation of lungs & decrease in neural drive to diaphragm


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea Dyspnea without primary lung disease

eg, HF a heightened resp drive secondary to expiratory flowlimitation or a peripheral m. reflex

eg, deconditioning similar phenomenon, exercise

training mediated in part by changes in peripheral m. function other conditions: could be accounted for by increased resp

drive resp m. weakness, late-stage pregnancy,

anemia, thyroid disorders, panic disorder,anxiety


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Mechanisms of DyspneaMechanisms ofMechanisms of DyspneaDyspnea role of afferent feedback from lungs & CW in

the genesis of dyspnea is complex RASRs (rapidly adapting strech receptors) atelectasis

Pulmonary C-fibers pulmonary edema

stimulate breathing & contribute to dyspnea via vagal stimulation alleviation of dyspnea via vagotomy or vagal blockade: consistent with

this concept

SASRs (slowly adapting strech receptors) lung inflationinhibit central resp drive & ameliorate dyspnea

immediate relief of dyspnea with thoracic movement following breath-holding BUT without improvements in ABG status: consistent with thisconcept

receptors outside the chest cold air blowing on face


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Diagnostic Approach of DyspneaDiagnostic Approach ofDiagnostic Approach of DyspneaDyspnea Intermittent dyspnea reversible conditions

eg, bronchoconstriction, HF, pleural effusion, acute PTE,

hyperventilation syndrome

Persistent/progressive dyspnea chronic conditions eg, COPD, interstitial fibrosis, chronic PTE, dysfunction of diaphragm

or chest wall

Nocturnal dyspnea

eg, asthma, HF, GER, OSA, nasal obstruction

Dyspnea in the recumbent position (orthopnea)

eg, left ventricular failure, abdominal processes (ascites),diaphragmatic dysfunction

Dyspnea worsening in the upright position (platypnea)

eg, cirrhosis, interatrial shunts


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Diagnostic Approach of DyspneaDiagnostic Approach ofDiagnostic Approach of DyspneaDyspnea To simplify conceptualization of the

pathophysiology of dyspnea, 3 components can be

independently discerned (multifactorial) WOB:

Increased effort required for breathing against increased resistance,eg COPD

OR breathing w/ weakened muscles, eg NMD, cachexia

Chemical:

Medullary chemoreceptors predominantly sense hypercapnia

Carotid & aortic chemoreceptors preominantly sense hypoxemia

Hypoxemia seems to have a less significant role than hypercapnia indyspnea

Neuromechanical dissociation

Mismatch btw what brain desires for resp & sensory feedback it receives,

dyspnea is increased


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Symptomatic Tx of DyspneaSymptomaticSymptomatic TxTx ofof DyspneaDyspnea

Reducing respiratory effort & improvingrespiratory m. function

Decreasing the respiratory drive

Altering central perception

Exercise training


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Symptomatic Tx of DyspneaSymptomaticSymptomatic TxTx ofof DyspneaDyspnea Reducing respiratory effort & improving

respiratory m. function

Energy conservation: pacing reduce physical effort Breathing technique: pursed-lip slowing breathing &

impoving O2 saturation

Strenthening resp. m. improve max. ventilation &exercise performance, esp. documented resp m weakness

Nutritional repletion improve resp m strength, espcachectic pt

NIV improve exercise performance in COPD, not in HFnocturnal bilevel nasal ventilation: more effective in NMDthan obstructive lung dz

Medication: theophylline increase m contractility, esp

persistently dyspneic COPD


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Symptomatic Tx of DyspneaSymptomaticSymptomatic TxTx ofof DyspneaDyspnea Altering central perception

Education including m relaxation understand their dz& develop feelings of mastery over it

Psychotherapy reduce intensity of dyspnea & distressassociated with it

Central acting agents: limited role in treating dyspnea Anxiolytics: no benefit for unselected COPD, useful in selected

COPD /c psychiatric disorder

Antidepressants: sertraline, amitriptyline may have positive result

Opiates: reduce dyspnea in ventilation /c exercise or hypoxia,affect an individuals experience as they do pain, inhalation ofopiates anecdotally to help pt with terminal lung dz, HF, terminalmalignant dz. BUT, controlled studies have been disappointing.

IV morphine alleviate dyspnea of acute LVF


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Symptomatic Tx of DyspneaSymptomaticSymptomatic TxTx ofof DyspneaDyspnea Exercise training

A critical part of pulmonary rehabilitation program

Decrease dyspnea even when exercise performance or

mechanical efficiency is not improved

Treadmill training/c or /s nurse coaching: equallyeffective in reducing dyspnea during exercise testing and

during ADL Many mechanisms (neither pul mechanics nor resp m strength is usually

affected)

True conditioning with decreased lactate production & resulting

decreased stimulation of ventilation Relaxation & increased mechanical efficiency: lower O2

consumption & ventilation

Improve self-confidence, thereby reducing anxiety & dyspnea

Desensitization of repeated exercise


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Indications for O2 TherapyIndications for O2 TherapyIndications for O2 Therapy Short-term O2 therapy

Tissue hypoxia /c arterial hypoxemia most common, esp VQmismatch

Tissue hypoxia /c normal PaO2 PaO2 is an inadequate indexof the need for O2 therapy

Acute myocardial infarction double-blinded studies of value ofO2 in uncomplicated MI demonstrated no significant effects onmorbidity or mortality

Inadequate CO (low-flow states) no proof, used in conjunction/c inotropes & other devices

Trauma & hypovolemic shock best treated by increasingsupply of circulating Hb

Carbon monoxide intoxication

Miscellaneous disorders: sickle cell crisis, pneumothorax


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Indications for O2 TherapyIndications for O2 TherapyIndications for O2 Therapy Long-term O2 therapy

Most are pt /c arterial hypoxemia, COPD represent the largestgroup of pt

Continuous supplemental O2 for 4-8 wks decreased Hb,improved exercise tolerance, lowered pul vascular pressures

Nocturnal O2 (> 15h/d) is better than O2, continuous O2 imparts the

most benefit Resting hypoxemia from a variety of cardiopulmonary dz: eg,

restrictive lung dz, cystic fibrosis, chronic cardiac dz

Exercise-induced hypoxemia improves exercise endurance,

as measured by either treadmill walking or bicycle ergometry Hypoxemia during sleep: eg, primary sleep-disordered breathing

(OSA, OHS), primary lung dz exhibiting nocturnal desaturation


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Techniques of O2 administrationTechniques of O2 administrationTechniques of O2 administration Choice of delivery system, based upon

Degree of hypoxemia Requirement for precision of delivery

Patient comfort

Cost The devices discussed below are reserved

primarily for conscious pt


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Techniques of O2 administrationTechniques of O2 administrationTechniques of O2 administration Oxygen delivery system in acute setting

Rebreathing is avoided through use of one-way valveto sequester expired from inspired gases

Inspired gas mixtures must be presented in sufficientvolume & at flows to allow compensation for the high-

flow demands often exhibited by critically ill pt

Can deliver humidified, heated inspired gases

Low-flow oxygen devices

High-flow oxygen devices


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Low-Flow Oxygen devicesLowLow--Flow Oxygen devicesFlow Oxygen devices


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High-Flow Oxygen devicesHighHigh--Flow Oxygen devicesFlow Oxygen devices


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High-Flow Oxygen devicesHighHigh--Flow Oxygen devicesFlow Oxygen devices


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Clinical Syndromes of O2 ToxicityClinical Syndromes of O2 ToxicityClinical Syndromes of O2 Toxicity Acute toxicity: tracheobronchitis & ARDS

Normal vlunteers exposed to 100% O2 in 12-24h Earliest: effects on tracheobronchial mucosa substernal

chest pain, nonproductive cough, decreased particleclearance as early as 6h

Systemic symptoms: malaise, nausea, anorexia, headache Latest: severe dyspnea, marked decrease in pul function,

acute resp failure, longest report is 110h

Chronic pulmonary syndrome

Newborns: NRDS /c O2 Tx bronchopul. dysplasia

Adults: can tolerate 100% O2 at sea level for 24hwithout serious pulmonary injury


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pa tho physiology of dyspnea & its treatment-20090320

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