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1 Waiting to Exhale Respiratory Disorders Peggy Andrews, Instructor Fall, ‘08.

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1 Waiting to Exhale Respiratory Disorders Peggy Andrews, Instructor Fall, ‘08
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Page 1: 1 Waiting to Exhale Respiratory Disorders Peggy Andrews, Instructor Fall, ‘08.

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Waiting to Exhale

Respiratory Disorders

Peggy Andrews, Instructor

Fall, ‘08

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A quick review

• Upper airway– To larynx– Warms,

humidifies, cleans– Cilia– Turbinates– Cribiform plate

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Review, continued

• Lower airway– Below larynx– Trachea– Bronchi– Alveoli– Surfactant

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Lower airway, cont.

• Lungs– Lobes– Visceral pleura– Parietal pleura

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Review, continued

• Ventilation– Inspiration– Expiration

• Respiration-Tidal Volume– 500ml

• Inspiratory Reserve Volume– 3000ml

• Expiratory reserve volume– 1500ml

• Residual volume– 1200ml

• Dead air space– 150ml

• Minute volume– TV x RR

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What controls our breathing?

• Medulla– 12-20/min

• Transmitted through – phrenic nerves

• 3rd, 4th, 5th spinal nerves

– and intercostal nerves• 11 pair

• Can be modified by – Cerebral cortex– Hypothalamus– Brainstem (pons)

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What controls our breathing, cont.

• Stretch receptors– Visceral pleura– Bronchi and bronchiole walls

Hering-Breuer reflex

Phrenic and intercostalnerves

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More stuff

• PCO2 increase = increased PCO2 in CSF = decreased pH

Respiratory patternsCheyne-StokesKussmaul’sCentral neurogenic hyperventilationAtaxic (Biot’s) Apneustic

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Cheyne-stokes

Central neuro-genic hypervent.

Apneustic

Ataxic (Biot’s)

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Respiratory Disorders

• Incidence - 28% of all EMS C/C

• Morbidity/Mortality - >200,000

deaths/yr.

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Risk Factors

• Stress

– Increases

severity of

respiratory

complaints &

frequency of

exacerbations

Genetic predispositionAsthmaCOPDCarcinomas

Assoc.

Cardiac

or circ

ulatory

pathologies

Pulmonary

edem

a

Pulmonary

emboli

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Case Presentation One

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Entering the bathroom, the EMTs find:

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The Patient Is:

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• 1. What is her differential diagnosis?

• 2. What treatment might you provide

for this patient? Why?

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Signs of life-threatening respiratory distress in adults

• Altered mental status

• Severe cyanosis

• Absent breath sounds

• Audible stridor

• 1-2 word dyspnea• Tachycardia >

130/min.• Pallor and

diaphoresis• Retractions/

accessory muscle use

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COPD

• Outflow obstructive diseases

– Emphysema

– Chronic Bronchitis

– Asthma

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The COPD patient

• May have any or all three diseases• Works harder to breath – tires

quickly• Be prepared to take over breathing

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Case Presentation Two

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You note the following:

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• What is his differential diagnosis?

• What treatment might you provide

him?

• Why?

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Emphysema

• Irreversible airway obstruction

• Diffusion defect also exists because

of blebs - prone to collapse - pt.

exhales with pursed lips

• Almost always associated with

cigarette smoking or environmental

toxins

                                                                             

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Xray of pt

With Emphysema

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Pathophysiology

• Stiffening and enlargement of alveoli – requires higher lung pressures

• More common in men• Walls of alveoli gradually destruct, =

alveolar membrane surface area. Results in ratio of air to lung tissue.

• Pulmonary capillaries , = resistance to pulmonary blood flow.

• Causes pulmonary hypertension, leads to RHF, then Cor Pulmonale

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Pathophys. (Cont.)

• Bronchiole walls weaken, lungs lose elasticity, air is trapped. Residual volume, but vital capacity relatively normal.

• PaO2 , = RBC, polycythemia.• PaCO2 , is chronically elevated. The

body depends on hypoxic drive.• Pt’s are more susceptible to pneumonia,

dysrhythmias.• Meds; bronchodilators, corticosteroids,

O2.

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Assessment• Altered mentation• 1-2 word dyspnea• Absent or decreased breath

sounds• c/c Dyspnea, morning cough,

nocturnal dyspnea, wheezing

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• History - – Personal or family hx of

allergies/asthma– Acute exposure to pulmonary

irritant– Previous similar expisodes– Recent wt. loss, exertional

dyspnea– Usually > 20 pack/year/history

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Exam

• Wheezing• Retractions

and/or accessory muscle use

• Barrel chest• Prolonged

expiratory phase• Rapid resting

respiratory rate

• Thin• Pink puffers• Clubbing of

fingers• Diminished breath

sounds• JVD, hepatic

congestion, peripheral edema

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Management

• Pulse oximeter• Intubation prn• Assisted ventilation prn• High flow oxygen• IV therapy with fluids• Albuterol, or Albuterol/Atrovent

neb• Transport considerations

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Chronic Bronchitis

• Productive cough for at least 3 months for two or more consecutive years

• An increase in mucous-secreting cells• Characterized by large quantity of

sputum• Chronic smoker• Alveoli not severely affected - diffusion nl. gas exchange = hypoxia & hypercarbia• May increase RBC = polycythemia paCO2 = irritability, h/a, personality

changes, intellect. paCO2 = pulmonary hypertension &

eventually cor pulmonale.

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Xray of pt

With Chronic

Bronchitis

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Assessment• Hx heavy cigarette smoking• Frequent resp. infections• Productive cough• Overweight, possibly cyanotic -

blue bloaters• Rhonchi on auscultation -

mucous plugs• S/S RHF; JVD, edema, hepatic

congestion

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Management

•Pulse oximetry•Oxygen - low flow if possible•Nebulized Albuterol/Atrovent •Constantly monitor•Position - seated•IV TKO

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Case Presentation Three

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You find the following:

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• What is your differential diagnosis?

• What treatment would you offer this patient and why?

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Asthma

• Reversible obstruction caused by combination of smooth muscle spasm, mucous, edema

• Exacerbating factors - extrinsic in children, intrinsic in adults

• Status asthmaticus - prolonged exacerbation - doesn’t respond to therapy

• Significant increase in deaths in last decade- 45 years or older - black 2x higher

• 50% are prehospital deaths.

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Pathophysiology• A chronic inflammatory airway

disorder.• Triggers vary - allergens, cold air,

exercise, food, irritants, medications.

• A two-phase reaction

Page 57: 1 Waiting to Exhale Respiratory Disorders Peggy Andrews, Instructor Fall, ‘08.

• Phase one– Histamine release - bronchial

constriction, leakage of fluid from peribronchial capillaries = bronchoconstriction, bronchial edema.

– Often resolves in 1 - 2 hours

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Pathophysiology (cont.)

• Phase two– 6-8 hours after exposure, inflammation

of bronchioles - eosinophils, neutrophils, lymphocytes invade respiratory mucosa; = additional edema, swelling.

– Doesn’t typically respond to inhalers; often requires corticosteriods.

• Inflammation usually begins days/weeks before attack.

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Assessment• Dyspnea, 1-2

word dyspnea• Persistent, non-

productive cough• Wheezing• Hyperinflation of

chest• Tachypnea,

accessory muscle use

• Pulsus paradoxis– 10-15 mm bp drop

during insp vs exp

• Agitated, anxious• Decreased

oxygen saturation• Tachycardia• Hx of allergies• Auto PEEP• Potential tensions

(bilateral)

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Management

• Check home meds• Determine onset of sx & what pt. has

taken• Check vitals carefully - resp. x 30 sec.• High flow oxygen• IV with fluids• ECG• Inhalers• Consider epinephrine 1:1,000 SQ, 0.3-0.5

mg • Consider Solu-Medrol, 1 –2 mg/kg IVP,

max 125 mg

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Status Asthmaticus

• Severe, prolonged asthma attack not responsive to tx.

• Greatly distended chest• Absent breath sounds• Pt. exhausted, dehydrated, acidotic.• Treat aggressively if obtunded,

profuse diaphoresis, floppy – Intubate (poss. RSI)

• Transport immediately

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Xray of a pt

With Asthma

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Case Presentation Four

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Your exam reveals the following: 

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• What is his differential diagnosis?

• What treatment would you offer

this patient? Why?

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Pneumonia• 5th leading cause of death in US• Risk factors

– Cigarette smoking– Alcoholism– Cold exposure– Extremes of age

Page 71: 1 Waiting to Exhale Respiratory Disorders Peggy Andrews, Instructor Fall, ‘08.

• Pathophysiology– A common respiratory disease

caused by infectious agent. bacterial and viral pneumonia most frequent.

– May cause atelectasis– May become systemic = sepsis

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Assessment• Typical

– Acute onset of fever and chills– Cough productive with yellow/green

sputum (bad breath!)– May have pleuritic chest pain– Pulmonary consolidation on

auscultation– Rales – Egophony (strange lung sounds)

• Atypical– Non-productive cough– H/A– Fatigue

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Management

• Position• Oxygen• Consider breathing tx.• IV with fluids• Cool if febrile• Elderly, over 65 years

– Significant co-morbidity– Inability to take meds– Support complications

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Xray of a pt

With

pneumonia

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Case Presentation Five

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On physical exam:

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• What is your differential diagnosis?

• What treatment would you offer

this patient? Why?

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Hyperventilation Syndrome

• Multiple causes– Hypoxia– High altitude– Pulmonary disease– Pneumonia– Interstitial pneumonitis, fibrosis,

edema– Pulmonary emboli– Bronchial asthma– Congestive heart failure– Hypotension– Metabolic disorder– Acidosis

               

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Hyperventilation Syndrome (cont)• Causes, cont.

– Hepatic failure– Neurologic disorders– Psychogenic or anxiety hypertension– Central nervous system infection,

tumors– Drug-induced– Salicylate– Methylxanthine derivatives– Beta-adrenergic agonists– Progesterone– Fever,sepsis– Pain– Pregnancy

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Assessment

• Chief complaint– Dyspnea– Chest pain– Other sx based on etiology– Carpopedal spasm– Tachypnea with high minute volume

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Management

• Depends on cause of syndrome

• Oxygen based on sx and pulse oximetry

• Consider coached ventilation

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Upper Respiratory Infection (URI)

• One of most common c/c• Usually viral• Bacterial infections

– Group A streptococcus• Strep throat• Sinusitis• Middle ear infections

• Most URI’s self-limiting

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URI continued

• S/S– Fever– Chills– Myalgias– Fatigue

• Tx– Supportive– Acetaminophen, ibuprofen, liquids

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URI, cont.

• If pediatric, beware of possibility of epiglotitis

• If PMH; Asthma or COPD, condition may worsen– Consider nebulized meds

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Lung CA

• Most caused by cigarette smoking• 4 major types

– Adenocarcinoma – most common• Origin; mucus-producing cells

– Small cell carcinoma– Epidermoid carcinoma– Large cell carcinoma

• Origin; bronchial tissues

• Most patients die w/in one year

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Lung CA, continued

• General Assessment;– Altered mentation– 1-2 word

sentences– Cyanosis– Hemoptysis– Hypoxia

• Advanced disease– Profound weight

loss– Cachexia– Malnutrition– Crackles, rhonchi,

wheezes– Diminished breath

sounds– Venous distention

in arms and neck

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• Localized disease– Cough, dyspnea, hoarseness, vague

chest pain, hemoptysis

• Local invasion– Pain on swallowing (dysphagia)– Weakness, numbness in arm– Shoulder pain

• Metastatic spread– Headache, seizures, bone pain,

abdominal pain, nausea, malaise

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Tx for Lung CA

• Oxygen prn• Support ventilations• Intubate prn• IV• Nubulized meds• DNR / Advanced directive?

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Toxic inhalation

• Consider if pt dyspneic• Causes

– Superheated air– Products of combustion– Chemical irritants– Steam inhalation

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Inhalation injury, cont.

• Medic safety– Ammonia (ammonium hydroxide)– Nitrogen oxide (nitric acid)– Sulfer dioxide (sulfurous acid)– Sulfur trioxide (sulfuric acid)– Chlorine (hydrochloric acid)

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• Assessment– Enclosed space?– Loss of consciousness?– Mouth, face, throat, nares– Auscultate chest– Laryngeal edema

• Hoarseness, brassy cough, stridor

• Management– Maintain airway– High-flow humidified oxygen– IV

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Carbon Monoxide inhalation

• Incomplete burning of fossel fuels, other carbon-containing compounds

• Automobile exhaust, home-heating devices most common causes

• CO has >200x affinity for hemoglobin– Cellular hypoxia

• Also binds to iron-containing enzymes– Increased cellular acidosis

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CO, continued

• Assessment– Source, length of exposure? Closed vs

open space?• S/S

– H/A, N/V, confusion, agitation, loss of coordination, chest pain, loss of consciousness, seizures

– Cyanosis– Cherry red (very late)

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CO, continued

• Management– SAFETY– Maintain airway– High flow oxygen (NRB vs assist– Hyperbaric oxygen therapy

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Pulmonary Embolus

• Thrombus• Ventilation perfusion mismatch• 50,000 deaths in US annually • Conditions that predispose to PE

– Recent surgery– Long-bone fracture– Bedridden– Long flights/truck drivers– Pregnancy– Cancer, infections, thrombophlebitis, Af,

sickle cell anemia– BCP

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PE, cont

• Assessment– Sudden onset SOB, Hypoxic– Pleuritic chest pain– Non-productive cough– History– Labored breathing, tachypnea,

tachycardia– RHF– DVT present

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PE, cont

• Management• ABC• Airway • High flow oxygen• ET?• IV – flow rate?• Heparin gtt? TPA?

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CT o

f Pul

mon

ary

Embo

lus

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Spontaneous pneumothorax

• Common- high recurrent rate– 5:1 male to female– Tall, thin– Smoking history– 20-40 years old– COPD = increased risk

• Ventilation perfusion mismatch if > 20%

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Spont. Pneumothorax, cont.

• Assessment– Sudden onset sharp chest or shoulder

pain– Coughing/lifting– Dyspnea– Decreased breath sounds at apex– Hyper resonance – Sub-cutaneous emphysema– Tachypnea, diaphoresis, pallor

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Spont. Pneumothorax, cont.

• Management– Supplemental oxygen – If sx increase, consider needle

decompression– Position of comfort

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Xray of

Spontaneous

Pneumothorax

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That’s all about breathingfor now, folks!

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