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IntroductionBreathing is easy: Air in, air out. It

seems pretty simple.But actually, it’s not.Breathing is part of a system – the

respiratory system – whose sum of itsinnumerable parts makes up thewhole. Knock out any individual part,and breathing falters.

As you know, the respiratory and thecardiovascular systems work togetherfor a mutual purpose: perfusion. Thebody’s billions of cells need a constantsupply of oxygen in order to createenergy needed for life. At the sametime, carbon dioxide, the waste pro-duct of metabolism, must be removedfrom the cells to prevent damage anddestruction. Perfusion, or cellular gasexchange, is essential to life.

This interdependent relationshipbetween the two systems is obvious,but actually all organ systems of thebody depend on the adequate func-tioning of the respiratory system, e.g.,endocrine, nervous, urinary, diges-tive, immune, lymphatic, etc. And,vice versa, the respiratory systemdepends upon all the body’s othersystems to adequately function. It’s anorgan-wide physiological “co-depen-dent” relationship without anybaggage!

This article is an “under the hood”piece, examining the nuts and bolts ofthis extraordinary engine we call therespiratory system. Although webriefly consider engine failure, it isprimarily about respiratory anatomyand physiology. (Note: Abnormal condi-tions are denoted with an asterisk.)

Gas In The Air Let’s first consider what’s in air

itself. The atmosphere – the wholemass of air surrounding you –con-tains 78.09% nitrogen, 20.95% oxygen,0.93% argon, 0.04% carbon dioxideand small amounts of other gases. (SeeFigure 1.) You inhale 20.9% oxygen;

you exhale 15.3%. Therefore, yourbody extracts or captures 5.6%oxygen.

Changes in the composition ofgasses in the atmosphere can lead toinadequate perfusion, and subsequent

hypoxia. For instance, if there is a massof carbon monoxide in the air,hemoglobin, the protein carrier in redblood cells, prefers to transport itinstead of oxygen. Consequently,oxygen is displaced by a poisonous gas.

Is adequate oxygen abundanteverywhere in the earth’s atmo-sphere?

At 7,000 feet above sea level, thepercentage of oxygen is the same, butthere are fewer oxygen molecules inthe air and the body’s O2 saturationbegins to plummet. The “thinner” airmeans there is less oxygen to breathe.To survive at high altitude, it’s neces-sary to breathe faster and deeper. *Theclimber needs to acclimatize to thechanges in air pressure and oxygenlevels by taking time (sometimes days)for her body to recalibrate the levelsof carbon dioxide and oxygen in thebloodstream. (See Figure 2 .) If shedoesn’t, she risks “altitude sickness,”e.g., headache, dyspnea, weakness,nausea, vomiting, etc. Symptoms may

What It Takes To Breatheby Julie Abergerby Julie Aberger

The Gold Cross CONTINUING EDUCATION SERIESThe Gold Cross CONTINUING EDUCATION SERIES

You inhale 20.9% oxygenand exhale 15.3%.

Therefore, your bodyextracts 5.6% oxygen.

You inhale 20.9% oxygenand exhale 15.3%.

Therefore, your bodyextracts 5.6% oxygen.

After reading this article, the EMT willbe able to:

• list structures and functions of theconduction and respiratory portions ofthe respiratory system;

• distinguish respiration fromventilation;

• explain the inverse relationship of gasvolume and pressure and how itaffects ventilation;

• understand some basic chemicalchanges that occur in the blood-stream that prompt the body tochange its respiratory pattern;

• identify normal as well as abnormalrespiratory rate, depth and conditions;

• understand the vital relationship ofpulmonary perfusion and ventilation.

After reading this article, the EMT willbe able to:

• list structures and functions of theconduction and respiratory portions ofthe respiratory system;

• distinguish respiration from ventilation;

• explain the inverse relationship of gasvolume and pressure and how itaffects ventilation;

• understand some basic chemicalchanges that occur in the blood-stream that prompt the body tochange its respiratory pattern;

• identify normal as well as abnormalrespiratory rate, depth and conditions;

• understand the vital relationship ofpulmonary perfusion and ventilation.

EMT ObjectivesEMT Objectives

Other Gases<1%

Figure 1:

Earth’s AtmosphereEarth’s Atmosphere

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be mild at 8,000 ft above sea level, butabove 12,0 0 0 ft , the affliction canbecome critical and even life threaten-ing, e.g., cyanosis, shortness-of-breathat rest, inability to walk, confusion,and pulmonary edema.

Conduction In order to move air to the lungs, we

look to the structures of the respira-tory system; all its parts must besound for the whole to function.(See Figure 3.)

The respiratory system can bedivided into the conducting portionthat conditions air – warms,humidifies, and filters it – before itreaches the bronchioles, and therespiratory portion where passivegas exchange occurs between thealveoli and the blood.

• Nasopharynx, oropharynx andpharynx, the vestibules of respira-tion: Air first enters the nose ormouth (or both) and moves into theback of the throat, or pharynx. *Thepassageway is wide; there’s plenty ofopportunity here for airwayobstruction, or aspiration: food,teeth, vomit, blood, bone, and secre-tions. But the most commonobstruction is the tongue. Whenyou lose consciousness, the musclesin your mandible relax, causing

your tongue to fall into the back ofyour throat, blocking your airway.

• Epiglottis: the structure thatcovers the windpipe when you areswallowing and opens when you arespeaking or breathing, a protectivedevice to keep food (and any other

foreign body) out of yourlungs.

*The epiglottis may fallforward and occlude theglottic opening when a patientis unconscious. *It can alsobecome infected and swell,and in case of epiglottitis, befatal. This condition can affectadults as well as children.

• Larynx, or voice box, iswhere air passes from thepharynx to the trachea .*Laryngospasm, a conditioncaused by smoke, asthma ,allergies, exercise or evenstress, can cause the larynx tosuddenly shut, closing off air.The patient may feel as if he ischoking and can’t breathe.*Gastroesophageal refluxdisease, or GERD, can alsoprovoke laryngospasm thatproduces stridor, the high-pitched breathing sound.

• Trachea, bronchi, bronchioles:The multi-passageways, or tubes,

from largest to smallest, that carry airto the alveoli.

*The trachea is about 4.3 incheslong, and an inch in diameter. Itextends from the sixth cervical verte-bra to the fifth thoracic vertebra. Itdivides into the right and left main-stem bronchi that further subdivideinto approximately 23 “generations,”or groups of branching airways. Thetrachea is kept open by 20 C-shapedcartilage rings. Between these rings, a

layer of smooth muscle allows forflexibility during inhalation and exha-lation. The two main stem bronchiand bronchioles are also lined withsmooth muscle that allows them toconstrict. *After prolonged contrac-tion, the muscle may suddenly spasm,narrowing, or completely constrictingthe airway. *The trachea, bronchi andbronchioles can become obstructed,infected, inflamed, and swell, occlud-

ing the passageway andincreasing the work ofbreathing. Infection alsocauses an increase inmucous production,decreasing the diameter ofthe airway and causingmore airway resistance.

A word about the grossanatomy of the lungs: Theycomprise five lobes, threeon the right, two on theleft. (See Figure 4, next page.)Anteriorly, both lungsextend from the base of theneck above the clavicle ofthe first rib, down to thesixth rib at the mid-clavic-ular line.

Respiratory Respiration is the pro-

cess by which oxygen and

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CEU Article: Respirations-continued from page 8

Laryngospasm, a condition caused by

smoke, asthma, aller-gies, exercise or evenstress, can cause the

larynx to suddenly shut,closing off air.

Laryngospasm, a condition caused by

smoke, asthma, aller-gies, exercise or evenstress, can cause the

larynx to suddenly shut,closing off air.

-continues on page 10

Figure 2:

Air/O2 Densities At AltitudesAir/O2 Densities At Altitudes

Figure 3:

The Respiratory SystemThe Respiratory System

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carbon dioxide diffuse in and out ofthe blood. It occurs in two areas of thebody. (See Figure 5.)

• External respiration refers to gasexchange in the alveoli, the 30 0million microscopic air sacs thatresemble clusters of grapes and makeup the lungs. (See Figure 6.) Their sur-faces secrete “surfactant” whichdecreases the surface tension betweenthe thin alveolar walls, and preventsthem from collapsing on exhalation.

• Internal respiration refers to gasexchange, or perfusion, that takesplace between the cells and the blood.

Pulmonary respiration takes placethrough diffusion; we inhale oxygen;we exhale carbon dioxide. The twogases diffuse simultaneously, goingfrom an area of greater concentrationto an area of lower concentration. Theoxygen then attaches itself tohemoglobin in the red blood cellsthat then carry it to the body’s cells.After the oxygen and other nutrientshave metabolized, the cell disposes ofthe waste product – CO2 – by sendingit back into the bloodstream to bedumped at the lungs. Carbondioxide can be transported back tothe lungs in three ways: dissolvedin plasma; chemically bound tohemoglobin; or converted to bicar-bonate ions in plasma.

How We Breathe: VentilationVentilation is the movement of

air into and out of the lungs.Inhalation is an active process thatdepends upon the contraction ofthe respiratory muscles, primarilythe diaphragm. Exhalation is apassive movement of air out ofchest that depends primarily onthe elasticity of the lungs. Both

adhere to Boyle’s Law of physics thatdefines how gases behave withrespect to pressure and volume.

Boyle’s Law says: “a volume of gas isinversely proportionate to the pres-sure.” The increase or decrease of thepressure within the chest cavity isdependent upon its internal size, orvolume. (Recall that the chest cavity isessentially a closed chamber.) Volumeleads to pressure changes that lead tothe flow of gasses to equalize thepressure.

• When you inhale, your dia-

phragm contracts, and moves down-ward, flattening. At the same time, theexternal intercostal muscles pull therib cage up and out. Both actionsincrease the size or volume of the spacewithin the chest cavity.

As the size or volume increases, theair pressure within decreases, andyou have a negative pressure, called apressure differential, i.e., a differencein air pressures. This leads to the flowof about 500 mL of air into the lungsuntil the intrapulmonary and atmo-spheric pressures equalize. Then,inhalation stops and exhalationbegins. As the respiratory musclesrelax passively, the elastic alveolirecoil, expelling the air up and out of

the lungs.Thoracic volume depends largely

on the diaphragm, the main muscleof respiration that longitudinallyseparates the thoracic cavity fromthe abdominal cavity. (Severalstructures pass through openingsin it: the aorta, the vena cava andthe esophagus.) When you inhale,the diaphragm contracts and flat-tens, increasing volume for thespongy lungs to inflate. When youexhale, the diaphragm relaxes andresumes its dome shape, decreasingvolume and squeezing air out ofthe lungs. The lungs, much likesponges, diminish in size.

The diaphragm depends on thebrain stem to control respirationsthrough the phrenic nerve, whichoriginates in the neck and descendsthrough the thorax to thediaphragm. *Traumatic injury tothe head or brain stem is oftencatastrophic to the phrenic nervedestroying respiratory control.*Other disorders that may criticallyaffect this essential muscle aredisease, and congenital and

CEU Article: Respirations-continued from page 9

Respiration is the processby which oxygen and

carbon dioxide diffuse inand out of the blood.

Ventilation is the movement of air into and out of the lungs.

Respiration is the processby which oxygen and

carbon dioxide diffuse inand out of the blood.

Ventilation is the movement of air into and out of the lungs.

Figure 4:

Five Lobes Of The Lungs Five Lobes Of The Lungs

Figure 5:

External/Internal RespirationExternal/Internal Respiration

Figure 6:

Gas Exchange In AlveoliGas Exchange In Alveoli

acquired anatomical development.The diaphragm can also be rupturedduring blunt force injury.

Accessory Muscles: What are they?And where are they found? Thesemuscles are the superchargers of therespiratory system that are used whenit is necessary to either inhale orexhale forcefully to get additional airin or out.

*For instance, consider a COPDpatient whose alveoli have lost theirelasticity and no longer recoil to expelair. To compensate, the patientengages his accessory muscles toexhale forcibly. (See Figure 7.) The con-tinuous additional muscular exertioncauses labored breathing and the dis-tinct facial flushing of “pink puffers.”

• Located in the neck, the sterno/cleido/mastoid (separated for easierreading) muscles and the scalenemuscles as well as other muscles inthe rib cage, provide strength whenyou forcefully inhale, increasing thevolume of air in your lungs.

• Located between the ribs: Whenyou exhale, the intercostal musclescontract and strengthen your abilityto quickly decrease the volume of airin your lungs.

You have eleven internal andeleven external intercostal muscles.Each rib is connected to the rib belowit by both an external and an internalintercostal muscle. (The twelfth rib isthe exception as it is the inferior-mostrib.) When you inhale, your externalintercostal muscles contract andelevate the ribs, spreading themapart. When you exhale, your inter-nal intercostal muscles pull the ribsdown and bring them closer together.The compression of the ribs

decreases the volume of the thoraciccavity, resulting in the forced exhala-tion of air from the lungs. (See Figure 8.)

• The abdominal muscles are nor-mally relaxed. But when you exhaleforcefully, they contract, pushing thediaphragm upward, and forcing theair out of the chest cavity.

Compliance, Resistance, Pleural Space, Minute Volume& Dead Space

What else must function for venti-lation to occur?

• Lung tissue must be compliant,that is, it must be able to stretch andcontinuously inflate and deflate. Thealveoli must be elastic enough torecoil and expel air. *Lung tissue canbe damaged by smoking, GERD,tuberculosis and pneumonia andexposure to toxic substances. Pul-monary fibrosis patients lose theirlung compliance after years of expo-

sure to toxic gases, and their air sacsstiffen. *Some emergency respondersworking at the World Trade Center in2011 suffered subsequent pulmonarydamage from toxic inhalation thatnecessitated lung transplants.

The structures in the thoracic cagemust also be flexible. *Aging cancause costal cartilages to ossify, orturn into bony tissue, which hinderschest expansion. *In COPD patients,the lungs become progressively morefibrous making ventilation difficult.

• The bronchi and bronchiolesmust be open and not occluded byobstructions such as mucus orswelling, commonly seen (and heard)in asthma and bronchitis patients.Resistance is determined by the inter-nal diameter of the lower airwaysleading to the alveoli. High resistancecan lead to dyspnea and apnea: Thepatient works harder to move air inand out, which causes him to tire andeventually, stop breathing.

• The (potential) space between theinner wall of the chest cavity – theparietal pleura – and the outer wall ofthe lung – the visceral pleura – mustbe intact.

There must also be adequate sur-factant, the serous fluid produced bythe alveoli that acts as a lubricantwhen the chest cage and lungs slidepast each other during ventilation.These two linings are in close contact;they have a molecular attraction and

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CEU Article: Respirations-continued from page 10

-continues on page 12

Thoracic volume depends largely on thediaphragm, the mainmuscle of respiration

that longitudinally separates the thoracic

cavity from the abdominal cavity.

Thoracic volume depends largely on thediaphragm, the mainmuscle of respiration

that longitudinally separates the thoracic

cavity from the abdominal cavity.

Figure 8:

Intercostal MusclesIntercostal Muscles

Figure 7:

Muscles of RespirationMuscles of Respiration

Inspiration Muscles

AccessorySternocleidomastoid(elevates sternum)

Scalenes(elevate upper ribs)

PrincipalExternal intercostals(elevate ribs,increasingwidth of thoraciccavity)

Diaphragm(domes descend,increasing verticaldimension of thoraciccavity; also elevatelower ribs)

Inspiration Muscles

Quiet BreathingExpiration results frompassive recoil of lungsand rib cage

Active BreathingInternal intercostals

Abdominals(depress lower ribs,compress abdominalcontents, push updiaphragm)

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oppose separation, like two flat wetpanes of glass stacked on top of oneanother. *If air enters the potentialspace between the two linings, thelung(s) loses its ability to inflate andthe patient becomes dyspneic. This iscalled a pneumothorax. (See Figure 9.)

How does a pneumothorax occur?A lung loses its integrity when it is

ruptured, resulting in either a closedor open injury. (The chest wall isintact in a closed pneumo, broken inan open. See Figure 10.) In a closedpneumo, the victim draws air into thelungs, which escapes through thehole into the pleural space betweenthe two linings. The air is trapped anddoes not escape on exhalation. Withevery breath, the presence of air inthe pleural space slowly exceeds thealveolar pressure, and the lung beginsto compress. As the patient continuesto inhale, the trapped air continues toamass and its pressure increasescausing the affected lung to collapse(atelectasis) and shift towards theunaffected side, eventually pushingthe heart, trachea, esophagus, andgreat vessels with it as well. This is atension pneumothorax. Blood flow-

ing into the chest cavity from an inter-nal injury can also accumulate in thisspace causing a hemothorax pneu-mothorax, aka hemo-pneumothorax.

• There must be an adequateminute volume. At rest, an averageadult inhales approximately 500 mLper breath at a rate of 12 breaths-per-minute. Minute volume is calculatedby multiplying the patient’s breaths-per-minute (12) times the amount ofinhaled air, or the tidal volume (500mL) 12 x 50 0 mL= 6,0 0 0 mL or 6liters/minute. Change the rate oramount of inspired air, and thepatient risks dyspnea.

• An adequate amount of air mustreach the alveoli. This is called alveolarventilation and it depends uponvolume and rate of respiration. Of the500 mL of air you inhale, only about350 mL reach the alveoli. About 150mL of air fill and remain in the deadspaces, such as the pharynx, larynx,trachea, bronchi and bronchioles. Ifthere are changes in the respiratoryvolume and/or rate, the alveolar ven-tilation is affected. If you ventilate apatient with too little volume, toolittle air reaches the air sacs, gasexchange is inadequate and thepatient becomes hypoxic.

Primary Drive toBreathe: ChemicalEquilibrium

Before we look at perfu-sion, we need to know onemore major fact about venti-lation. What activates the res-piratory system to breathe?

The primary drive tobreathe is based on the levelof CO2 in your arterial blood.If that fails, your respiratorydrive depends secondarily on

the level of oxygen in your arterialblood.

Your blood is kept in a chemicalequilibrium by “receptors,” or nerveendings that respond to particulartypes of stimuli. These specializedreceptors are found in the medulla inthe brainstem, and within the walls ofthe aortic arch and the carotid artery.

•The medulla contains centralchemoreceptors that are extremelysensitive to changes in the chemistryof the blood and cerebral spinal fluid.

• Chemoreceptors in the aorticarch and the carotid artery are calledperipheral chemoreceptors and areextremely sensitive to changes inoxygen levels. This is called hypoxicdrive. *A person who has smoked orbeen exposed to other toxic gases,may eventually lose the elasticity ofhis alveoli; the airsacs can no longerrecoil effectively to expel carbondioxide. Consequently, his body’s

“normal” arterial blood level of CO2becomes chronically elevated. Thecentral chemoreceptors, now desensi-tized to fluctuations in these gaslevels, finally fail.

This is when the secondary drive tobreathe kicks-in; the peripheralchemoreceptors now monitor thelevel of oxygen in the arterial blood.When the oxygen level is too low, therespiratory drive is stimulated andyou take a breath. This is called“hypoxic drive,” no doubt a familiarterm to most EMTs. When the oxygenlevel in the arterial blood is adequate,no breath is needed.

*You’re administering 15 lpmoxygen via nonrebreather to a patientwith an unknown history of emphy-sema when he suddenly quits breath-ing. What happened? By flooding the

CEU Article: Respirations-continued from page 11

Figure 9:

Three Types Of PneumothoraxThree Types Of Pneumothorax

Resistance is determinedby the internal diameter

of the lower airwaysleading to the alveoli.

High resistance can leadto dyspnea and apnea:

the patient works harderto move air in and out.

Resistance is determinedby the internal diameter

of the lower airwaysleading to the alveoli.

High resistance can leadto dyspnea and apnea:

the patient works harderto move air in and out.

The primary drive tobreathe is based on the

level of CO2 in your arte-rial blood. If that fails,your respiratory drive

depends secondarily onthe level of oxygen inyour arterial blood.

The primary drive tobreathe is based on the

level of CO2 in your arte-rial blood. If that fails,your respiratory drive

depends secondarily onthe level of oxygen inyour arterial blood.

Figure 10:

Open (Sucking) PneumoOpen (Sucking) Pneumo

system with almost 100% oxygen, thepatient’s stimulus to breathe – lowoxygen levels – is deactivated. Butnever withhold oxygen from a patient in res-piratory distress. In this case, be ready toventilate with a bag valve mask.

What happens when chemorecep-tors detect significant changes inblood gas levels? Truth is, the chem-istry is complex and too onerous toexplain in a short CEU article. But beaware, that when chemical imbal-ances occur, they prompt the body(the lungs and the kidneys) to reflex-ively take protective action, such aschanging the heart rate, respiratoryrate, and blood pressure, to restorehomeostasis. Here are some of theconditions our EMS patients experi-ence and we witness:

• An increase in CO2 triggers thecentral chemoreceptors to dump(expel) the excess gas. The brainsignals the body to increase its respi-ratory rate and depth to blow-offmore CO2. *Consider an elderlybedridden patient in a nursing homewhose breaths are slow and shallow.

After a time, she begins to retain CO2from hypoventilation. Eventually, herbreathing becomes abnormal, deep,rapid and labored in an attempt to ridthe body of excessive carbon dioxide.This is called Kussmaul breathing andoccurs in central nervous system dis-orders, diabetic ketoacidosis as well askidney failure.

• A decrease in CO2 produceshyperventilation. *When a patientexperiences anxiety or panic, andbreathes too deeply and rapidly(“excessive breathing”), too muchcarbon dioxide is removed from thebloodstream, leaving the cellsdepleted. Hypocapnia, or low arterialCO2, causes a chemical reaction thatcauses vasoconstriction of the cere-

bral blood vessels, and results inhypoxia. The patient feels confused,lightheaded, faint, has tingling in hishands and feet , and around hismouth as his muscles contract andspasm.

This patient does not need oxygen!He needs to restore his arterial CO2.In addition, check the patient’s pulseoximetry. If those numbers are good,the EMT should first urge him to slowhis breathing and coach him for aminute or so in doing it. No paperbags! There are other acute critical ill-nesses, like pulmonary emboli, thatact like hyperventilation. You need toknow patient history!

Ventilation/Perfusion RatioIn order for cellular perfusion to

occur, there must be adequate ventila-tion and blood flow, i.e., there must beenough blood flowing through the pul-monary capillaries while at the sametime, there must be adequate oxygen inthe alveoli during ventilation.

Let’s consider this vital relationshipbriefly:

The ratio that describes the amountof ventilation, or “V,” with the corre-sponding amount of perfusion, or“Q,” is V/Q. This ratio is never perfect(1-1). Conditions that cause alterationsof V/Q include gravity, pressure

imbalances and ventilation distur-bances.

• The apexes, or tops of the lungs,contain fewer alveoli, but they have agreater capacity than the alveoli at thebases. That means they can hold moreair, but because of gravity and surfacetension, make them less compliantand difficult to fill. The greatestamount of ventilation and corre-sponding blood flow occur in themore numerous alveoli in the bases.Consequently the bases are muchbetter perfused. *A good reason to keeppatients with inadequate breathing sittingup!

• Inadequate ventilation, resultingfrom bronchospasm or mucous plug-ging for example, leads to inadequategas exchange. There’s not enoughair/oxygen reaching the alveoli todiffuse into the capillaries.

• Inadequate perfusion, resultingfrom hypotension or pulmonaryemboli, for example, leads to inade-quate gas exchange. There’s notenough blood in the capillaries todiffuse with the oxygen in the alveoli.

*A patient who is hemorrhagingloses blood pressure; less blood isshunted through the capillaries creat-ing hypoperfusion.

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CEU Article: Respirations-continued from page 12

-continues on page 14

Hypocapnia, or low arte-rial CO2, causes a chemi-cal reaction that causesvasoconstriction of thecerebral blood vessels,and results in hypoxia.

Hypocapnia, or low arte-rial CO2, causes a chemi-cal reaction that causesvasoconstriction of thecerebral blood vessels,and results in hypoxia.

Inadequate ventilation,resulting from broncho-

spasm or mucous plugging, for example,

leads to inadequate gas exchange.

Inadequate ventilation,resulting from broncho-

spasm or mucous plugging, for example,

leads to inadequate gas exchange.Chemical imbalances

prompt the body to takeprotective action, such aschanging the heart rateand blood pressure, torestore homeostasis.

Chemical imbalancesprompt the body to takeprotective action, such aschanging the heart rateand blood pressure, torestore homeostasis.

Why Do I Have To Know A&P?What importance is all this nuts-

and-bolts information to an EMT?As you may remember, our 2009

National EMS Education Standardsomitted the “B” in EMT-B and wewere once again plain old EMTs. Theimplication now is that we arerequired to “think critically” beyondbasic protocols, and apply that think-

ing to clinical decisions. In order todo that, we must know more science,i.e., medicine, including pathophysi-ology. To do that, you must know theanatomy and physiology of thehuman body.

It’s vital to understand not onlywhat to do about an airway or breath-ing problem, but what is causing it.EMTs have been tasked with a higherduty, one that necessitates more studyand medical insight. Continual train-

ing and study are key.

Julie Aberger is an EMT instructor andan active member of the Pennington FirstAid Squad. Julie is also the editor emeritaof The Gold Cross.

Many thanks to my many friendswho helped with this article includingDr. Alice Freeman, Doug Kabay, JonPolitis, Andy Jefferson and readerJoan Schwarzwalder.

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CEU Article: Respirations-continued from page 13

• Normal respiratory rates in breaths-per-minute:Adult 12-20 Child 15-30Infant 25-50 Newborn 40-60

A patient with respirations less than 8 or more than 24 BPMneeds your immediate attention: she may need ventilation. Butfirst, consider history, i.e., what happened, or her chief complaint.Is the patient breathing rapidly because she’s in respiratory dis-tress or did she just jog several miles?

• Normal respiratory depth: Check for adequate chest expan-sion, its rise and fall. If breathing is shallow and the chest is barelyrising, the patient needs ventilation.

• Recognize inadequate breathing patterns: rapid, irregularbreathing is a sign of respiratory distress. Head injuries andstrokes may produce Cheyne-Stokes respirations; a repetition ofincreasing, decreasing then total cessation of breath which alonecan last up to a minute. Kussmaul’s respirations occur as deep,gasping breaths, commonly seen in patients trying to blow offexcessive CO2. Biot’s breathing occurs with increased intracranialpressure and produces two-to-three short breaths with long, irreg-ular periods of apnea. Agonal describes those last gasping breathsbefore death.

• Recognize signs & symptoms of respiratory distress orimpending failure: tripoding, labored breathing, use of accessorymuscles, inability to speak in full sentences, agitation, confusion,somnolence, and unconsciousness. Diminished or absent breathsounds are abnormal, so is the presence of rales, rhonchi andwheezing.

• Skin color and condition may be one of the most obvious signsof poor perfusion. A patient breathing inadequately may be cool,clammy and cyanotic.

Pink is good, blue is bad! If your patient is pale, ashen, or duskyblue or gray, give her oxygen.

• Oxygen Therapy:

*Pulse oximetry measures theoxygen saturation of arterial capil-lary blood. It can also be used tomonitor the effectiveness of theEMT’s oxygenation therapy (NC, NRBor BVM). This device is used as anadjunct to patient assessment! Itsresults alone are not significant.Conditions that may affect the pulse oxreading: hypothermia, hypovolemia, carbon monoxide or cyanidepoisoning, some fingernail polish, anemia, Sickle Cell disease, evenbright lights. A normal pulse ox reading falls between 96-100%.

*Adequate oxygen delivery to an adult with a bag-valve-maskdevice requires you to deliver 600 ml of air; squeezing two-thirdsof the bag over one second into the patient’s lungs every fiveseconds. Do not squeeze the bag too hard or too fast! Excess airends up in the belly, forcing the diaphragm upward and creatingmore difficulty breathing.

• Nasal cannulas are still used primarily when the patientcannot tolerate a nonrebreather mask. Used together with thepulse ox, they are currently also used for patients complaining ofchest pain, but no difficulty breathing. Nasal cannulas play a minorrole in EMS, and are actually designed for long-term hospital use.

A BIT OF BASIC RESPIRATORY REVIEWA BIT OF BASIC RESPIRATORY REVIEW