Waiting to Exhale - faculty at Chemeketa

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Transcript Waiting to Exhale - faculty at Chemeketa

Waiting to Exhale
Respiratory Disorders
1
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 and
intercostal nerves
• Can be modified by
– Cerebral cortex
– Hypothalamus
– Brainstem (pons)
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What controls our breathing, cont.
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More stuff
• PCO2 increase = increased PCO2 in CSF
= decreased pH
Respiratory patterns
Cheyne-Stokes
Kussmaul’s
Central neurogenic hyperventilation
Ataxic (Biot’s)
Apneustic
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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
Genetic predisposition
Asthma
COPD
Carcinomas
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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/accessor
y muscle use
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COPD
• Emphysema
• Chronic Bronchitis
• Asthma
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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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Pathophysiology
• Destruction of alveolar walls distal to
terminal bronchioles.
• More common in men
• Walls of alveoli gradually distruct, = 
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
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•
Altered mentation
1-2 word dyspnea
Absent 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
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•
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•
Thin
Pink puffers
Clubbing of fingers
Diminished breath
sounds
• JVD, hepatic
congestion,
peripheral edema
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Management
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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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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
• Albuterol inhaler
• 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 - intrinsic in children,
extrinsic in adults
• Status asthmaticus - prolonged exacerbation doesn’t respond to therapy
• Significant increase in deaths in last decade45 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
• Phase one
– Histamine release - bronchial contraction,
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, nonproductive 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
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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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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
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Cigarette smoking
Alcoholism
Cold exposure
Extremes of age
• 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
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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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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
• Causes, cont.
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(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
– Fatugue
• 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; • Advanced disease
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Altered mentation
1-2 word sentences
Cyanosis
Hemoptysis
Hypoxia
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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, mailaise
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Tx for Lung CA
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Oxygen prn
Support ventilations
Intubate prn
DNR / Advanced directive?
IV
Nubulized meds
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Toxic inhalation
• Consider if pt dyspneac
• 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
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Thrombus
Ventilation perfusion mismatch
50,000 deaths in US annually
Conditions that predispose to PE
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Recent surgery
Long-bone fracture
Bedridden
Long flights/truck drivers
Pregnancy
Cancer, infections, thrombophlebitis, Af, sickle cell
enemia
– 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
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Management
ABC
Airway
High flow oxygen
ET?
IV – flow rate?
Heparin gtt? TPA?
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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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