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conducting pathway:
Nasal cavity and sinuses
Pharynx
Larynx
Trachea
Nasal Cavity:
The nasal cavities are separate from each other
by the nasal septum.
Vascular membrane on the Nasal Septum
Most nose bleeds in young people originate at
the anterior nasal septum
Most nose bleeds in older people are from the
posterior nasal structures
The Cribriform plate is the thin layer of bone that
separates the brain from the nasal cavity.
Lungs:
Right Lung 3 lobes
Left lung 2 lobes
Bronchioles:
Smallest airways
Walls consist entirely of smooth muscle (No
cartilage present)
*Constriction increases resistance to airflow
Inspiration
Active process
Chest cavity expands
Intrathoracic pressure falls
Air flows in until pressure equalizes
*Needs to make PEEP (Positive end
expiatory pressure)
Create 5 tor/mg to maintain PEEP
Expiration
Passive process
Chest cavity size decreases
Intrathoracic pressure rises
Air flows out until pressure equalizes
Upper Airway:
Trauma
Epiglottis
FBAO
Inflammation of tonsils
Lower Airway:
Trauma
Obstructive lung disease
Mucus accumulation
Smooth Muscle spasm
Airway edema
Chest Wall Impairment:
Trauma
Hemothorax
Pneumothorax
Empyema
Pleural
Inflammation
Neuromuscular diseases
Neurological Control:
Brainstem dysfunction- Coning
Phrenic or spinal nerve dysfunction
Perfusion:
Inadequate blood volume or
hemoglobin
Hemmorging
Hypovolemia
Anemia
Impaired Blood Flow:
Pulmonary Embolus
Thoracic: (Ventilation)
Chest Trauma:
Flail Chest
Simple Rib Fracture
Pneumothorax
Hemothorax
Sucking Chest Wound
Diaphragmatic Hernia
Pleural effusion
Spinal Cord Trauma
(High C-spine lesion)
Morbid Obesity
Neurological/Neuromuscular Disease
Poliomyelitis
Myasthenia
Muscular dystrophy
Guillain-Barre Syndrome
Respiratory Pathophysiology:
Drive system (Decreased Respiratory
Drive)
Head Trauma
CVA- (Stroke) Around Pons & Maddule
Sedatives- Hypnotics
Ethyl Alcohol
Initial Assessment:
Airway
Anticipate airway problems with
Decreased LOC
Head Trauma
Maxillofacial Trauma
Neck Trauma
Chest Trauma
OPEN-CLEAR-MAINTAIN
Respiratory Sounds:
Respiration Requires:
Ventilation, the mechanical process of
Ventilation:
Tracheobronchial tree: involved in
ventilation but does not participate in gas
exchange.
Gas Exchange: Takes place in the
respiratory of the lungs, where gas
diffuses across the alveolar-capillary
membrane as they are exchanged
between the lungs and the blood that
flows through the pulmonary capillaries.
Regulation Of Respirations:
DEPENDS ON 5 COMPONENTS:
1.
Normal Respirations:
Vesicular: Low pitched (soft) breath
sounds that consist of a quiet. Wispy
inspiration phase with a shortened and
softer expiratory phase. They are
heard over the periphery of the lung
field.
Bronchovesicular: Louder (more
harsh), breath sounds consists of full
inspiratory phase with a shortened and
softer expiratory phase. They may be
heard throughout the full lung field and
are often louder than tracheal breath
sounds.
Low Rate
High Rate
30
60
Toddler (1-2
yrs)
24
40
Preschooler
(3-5 yrs)
22
34
School age
(6-12 yrs)
18
30
Adolescent
(13-18 yrs)
12
26
12
20
Respiratory System:
Tachypnea/Bradypnea:
Orthopedic?
Signs of Respiratory Distress:
Nasal Flaring (Opening up Airway as
much as possible)
Tracheal Tugging
Reactions
Accessory Muscle use
Use of abdominal muscle on exhalation
Tripod Positioning
Sniffing position- angle
Respiratory Assessment:
Cyanosis (Late, unreliable sign of
Hypoxia)
OXYGENATE Immediately! Especially if:
Decreased LOC (first Sign)
Possible Shock
Possible severe Hemorrhage
Chest Pain
Chest Trauma
Respiratory Distress or Dyspnea
Pulmonary Embolism:
50,000 deaths/year
5% of all sudden deaths
10% of PE result in death
Cancer
Long flights
*Polycythemia: Increase in Red Blood
Cells
Anemia due to poor perfusion
Training lower partial pressure in
certain states
Training: Anticoagulability given
Other Causes:
Air
Amniotic Fluid (mom can leak
fluid into vascular)
Fat Particles (long bone fracture)
Particles from substance Abuse
Venous Catheter
Signs & Symptoms Of PE:
RAPID ONSET
DYSPNEA
TACHYCARDIA
TACHYPNEA
FEVER (SOMETIMES)
EPISODIC (SHOWERS)
EVIDENCE OR HISTORY OF
THROMBOPHLEBITS (Plaque)
CONSIDER EARLY WHEN NO OTHER
CARDIORESPIRTORY FITS
V:
VERY LARGE EMBOLI
Preceded by s/s of small & larger
emboli:
Central Chest Pain
JVD
ACUTE RIGHT HEART FAILURE:
Blockage right heart failure
Shock
Cardiac Arrest
ARDS:
A condition that results in severe
illness or injury and associates
with a high mortality rate
Increased permeability
Pulmonary Edema
Surfactant Destruction
Atelectasis
Decreased compliance
Hypoxemia (severe Hypoxemia)
Blood O2 low
ADULT RESPIRTORY DISTRESS
SYNDROME:
AKA: NON-Cardiogenic Pulmonary
edema
A Complication Of:
Severe Trauma/Shock
Severe infection/sepsis
Bypass Surgery
Multiple Transfusion
Drug Overdose
Aspiration
Decreased compliance
Hypoxemia: Fluid in alveoli, gas
exchange is embedded, cannot
perfuse, alveoli
ARDS MANAGEMENT:
Airway Management:
Endotracheal Intubation
Suction
MECANICAL VENTALTION:
PEEP
ECG Monitoring:
Treat Under lying Causes:
May require Vasopressors for shock
C-PAP
B-PAP
Splint Alveoli PEEP Ventilation
PNEUMONIA:
PNEUMONIA:
Inflammation of Bronchioles and
Alveoli
Products of inflammation (secretions,
pus) add to respiration difficulty
Presentation Of Pneumonia:
Shortness of breath, Dyspnea
Fever, Chills
Pleuritic Chest Pain, Tachycardia
Cough
Green/Brown Sputum
May have crackles, rhonchi,
wheezing in peripheral lung fields
Consolidation
Egophony
Management Of Pneumonia:
Allergens
Drugs
Occupational Hazards
General Pathophysiology:
Specific pathophysiology varies by
disease
Obstruction in Bronchioles
Smooth muscle spasm (beta0
Mucus accumulation (Goblet cells get
irritated and mucus)
Inflammation
Obstruction may be reversible or
irreversible
Obstruction results in air trapping
Bronchioles usually dilate on
INSPIRATION
Dilation allows air to enter even in
presence or obstruction
Bronchioles tend to CONSTRICT on
expiration
alveoli/muscles
Destruction of Alveolar walls
Distention of pulmonary air space
Destruction of gas exchange surface
Alveoli get stretched due to air
Descent
Geriatrics Disease
PATHOPHYSIOLOGY:
Decreased surface area leads to
decreased gas exchange with blood
Loss of pulmonary capillaries &
Hypercarnia Leads to:
Increased resistance to blood flow
which leads to:
Pulmonary HTN
Right Heart Failure (Cor Pulmonale)
Loss of elastic recoil leads to increase
in residual volume and CO2 retention
Air trapping
Hyperinflation
Hypercapnia
Vasoconstriction
Pulmonary
V/Q
mismatch
SIGNS AND SYMPTOMS:
Increased Thoracic AP Diameter (Barrel
Chest)
Decreased Lung sounds/ heart (size of
surface area increased
Hyperresonant chest
LIP PURSING: Air Trapping to increase
PEEP levels (exhalation)
Alerted blood gases
Normal or decreased PaO2
Elevated CO2
Clubbed fingers
Still perfusing
Cyanosis is a late sign of disease
PINK PUFFER!
Treatment:
BLS:
Ventilate
O2 mask
Cardiac Monitor Irregular (PVC)
Monitor Breathing
Chronic Bronchitis:
Increased mucus production for more
then 3 months for 2 consecutive years.
Recurrent productive cough
Etiology:
Smoking
Environmental irritants
Pathophysiology:
Mucus plugging/inflammation edema
Increase airflow resistances leads to
alveolar hypoventilation
Alveolar Hypoventilation leads to:
Hypercardia
Hypoxemia
Dont air trap
Hypoxemia leads to: Increase in red
blood cell production without O2
causing Cyanosis: Barrel and
Chemoreceptors tell to increase/ not
getting enough red blood cells,
PITTING EDEMA
Personality Change
Hyperocarbia
Hypoxia
Fluid Backs up, Inferior and Superior
become semi-permeable, blood leaks
out into interstitial space
Treatment: * Antibiotics
CYANOSIS IS AN EARLY COURSE OF
DISEASE
BLUE BLOATER!!
COPD Assessment Findings:
Chronic Condition
Acute
Episode
S&S of
work of breathing
and/or hypoxemia
Use of accessory muscles
Increased expiratory effort
Tachycardia
Cyanosis
Wheezing, Rhonli
Understand Difference!
Respiratory Failure:
Inability of the lungs to meet metabolic
demands of the body
Cant take in enough O2 & Cant
eliminate enough CO2 fast enough
Ventilation Failure: Imbalance between
load on the lungs and the ability of the
bellows to compensate
Failure of Oxygenation: PaO2 <60
mmhg
Failure to Ventilation: PaCO2 >50
mmhg
ARDS:
Leaky Alveolar capillaries
Plasma fluid and Leukocytes leak into
the airspace
Shunt
Hypoxemia
CAUSES OF ARDS:
Pneumonia
Aspiration of Gastric contents
Pulmonary Contusion
Near-Downing
Inhalation Injury (CO-Smoke)
Reperfusion Pulmonary Edema
After Lung Transplant or
Pulmonary Embolectomy
INDIRECT LUNG INJURY:
Non-Pulmonary sepsis
Severe trauma with SHOCK
Cardiopulmonary Bypass
Acute Pancreatitis
Drug Reaction (ARA-C)
FAT, Amniotic Fluid
Embolism, bypass
PATHOPHYSIOLOGY:
Increase alveolar permeability due
to direct neutrophil-mediated
injury to the alveolar epithelium.
Always ends in some form of
fulminating Edema.
End result:
Severe HYPOXEMIA
BLS THEARPHTIC GOALS:
Maintain Reasonably Oxygen
Delivery
FIND & FIX PRIMARY CAUSE
THORACIC TRAUMA:
Second leading cause of trauma
deaths after head injuries
Causes of about 10-20% of all auma
death
Many deaths due to thoracic trauma
are preventable
PREVENTION STRATEGIES:
Gun Safety Education
Sports Training & Protective
Equipment
Seat Belts & Air Bag Use
Mechanism Of Injury
Blunt Injury
Deceleration
Compression
Penetrating Injury
Both
Anatomical Injuries:
Thoracic Cage (Skeletal)
Cardiovascular (Lethal Dysrhythmia)
Pleural and Pulmonary Mediastinal
Diaphragmatic
Espogheal
Penetrating Cardiac (Grave TOR)
Often Results in:
Hypovolemia
Pulmonary V/P mismatch
In intrathroxic pressure relationships
(external signs breathing, JVD, angle
stretcher 30 degrees, pressure up,
Pain
Air in pleural sac
Asymmetrical movement
Bleeding in Pleural Space
Ineffective Diaphragm contraction
Impairment in Gas Exchange:
Atelectasis
Pulmonary Contusion
Respiratory Tract disruption
Initial Exam directed towards
Open Pneumothorax
Flail Chest
Tension Pneumothorax
Massive Hemothorax
Cardiac Tamponade
Conditions:
Apnea
Respiratory Distress
ASSESSMENT FINDINGS:
Mental Status (decreased)
Pulse (Absent, Brady, Tachy)
BP (Narrow PP, Hyper/Hypotensive)
Pulsus Paradoxus: Alteration in BP in
inspiration
Ventilation rate & effort (Tachy, or
Brady, Labored, retractions)
Skin (Diaphoresis, pallor, Cyanosis, open
injury, ecchymosis)
Neck (Tracheal position, SQ
emphysema, JVD, Open Injury)
Chest (contusions, tenderness,
asymmetry, absent or decreased lung
sounds, abnormal percussion, open
high force
Frequently have injury to aorta or
bronchi
Occur in 90% of patients with
Tracheo-Bronchial rupture
Subcutaneous emphysema)
May injure Subclavian artery/vein
(nerve under Clavicle)
May result in Pneumothorax
30% will die
Fractures to the 9th to 12th ribs
can cause damage to underlying
abdominal solid organs:
Liver
Spleen
Kidney (Blood in Urine)
associated injuries
Mortality increased with:
Seven or more ribs fractured
Three or more associated injuries
Shock
Head Injuries
CONSEQUENCES OF FLAIL
CHEST:
Respiratory Failure due to:
Pulmonary Contusion
Intrathoracic Injury
Inadequate diaphragm movement
PARADOXICAL MOVEMENT:
Must large to compromise
ventilation
Increased work of breathing
EMERGENT TRANSPORT:
TRUAMA CENTER
SIMPLE Pneumothorax:
Pleural wall
Incidence:
10-30% in blunt chest trauma
almost 100% with penetrating chest
trauma
Morbidity & Mortality depends on:
Extent of atelectasis
Associated Injuries
CAUSES:
Commonly a fx rib lacerates lung
Paper bag effect
May Occur spontaneously in tall,
thin, young males following:
Exertions
Coughing
Air Travel
Spontaneous may occur with
Marfans Syndrome (Elongated
Lungs)
PATHOPHYSOLOGY:
breathing deeply
MANAGEMENT:
Establish airway,
Trend Vitals
Dont leave patient alone
High Conc. O2
Assist with BVM
Decreased or rapid respirations
Inadequate Tidal Volume (TV)
IV or LS/NS
Monitor Progression
Monitor ECG
Usually non-emergent transport
Acidotic
Open Pneumothorax:
Hole in chest wall that allows
air to enter pleural space
(One Side)
Inability to ventilate affected lung
V/Q mismatch:
Shunting
Hypoventilation
Hypoxia
Large functional dead space
EMERGANT TRANSPORT-TRAUMA
CENTER
TENSION PNEUMOTHORAX:
Incidence:
Penetrating trauma
Blunt Trauma
Morbidity/Morbidity: High
Severe Hypoventilation
Immediate Life-threat if not
managed early
Cant treat this
Recognize
30 minute transport-Heli- Rapid
Pathophysiology:
One-way Valve forms in lung or
chest wall Air enters Pleural Space,
but cannot leave
Air is trapped in pleural space
Pressure collapses lung on affected
side
Mediastinal shift contralateral side
late)
JVD
Absent if hypovolemic
Hyperresonance to percussionIntercostal in-between ribs (tap)
SQ emphysema
TRACHEAL SHIFT AWAY FROM
INJURED SIDE (late)
Cyanosis (late)
MANAGEMENT:
Recognize & Manage early
Establish Airway
High O2
Positive pressure ventilation with
BVM
Needle thoracostomy
Iv of LR/NS
Monitor ECG
EMERGENT TRANSPORT
Consider need to intubation
Trauma center
Hemothorax:
PATHOPHYSIOLOGY:
Blood in Pleural space
Most common as a result of major
chest trauma to the chest wall
Present in 70-80% of penetrating
and major non-penetrating trauma
cases
Associated with Pneumothorax
Rib fractures are frequent causes
Blood vessels ruptures
Blood in 1000cc-3000cc
Flat Neck Veins
*Kinematics Higher
Each can hold up to 3000cc of blood
Life-threatening often requiring
Space
Penetrating or blunt trauma
Chest wall vessels
Intercostal vessel
Myocardium
MASSIVE hemothorax indicates
Tachypnea or Respiratory
Distress
Shock
Rapid, weak pulse
Hypotensive, Narrow PP
Restlessness, Anxiety
Cool, Pale, Clammy Skin
Thirst
Pleuritic Chest Pain
Decreased Lung sounds
Collapsed neck veins
Dullness on Percussion
MANAGAEMENT:
Establish Airway
High Conc. O2
Assist ventilations with BVM
MAST in Profound Hypotension
Needle Thoracostmy if tension &
unable to differate from Tension
Pneumothorax
IVs X2 with LR/NS
Monitor ECG
trauma:
30-75% of blunt trauma
Mortality 14-20%
Rib fx in many but not all cases
Alveolar rupture with hemorrhage 7
Edema
Increased capillary membrane
permeability
Large vascular shunt develop
Gas exchange disturbances
Hypoxemia
Hypercarbia
ASSESSMENT FINDINGS:
Tachypnea or Respiratory distress
Tachycardia
Evidence of blunt chest trauma
Cough and/or Hemoptysis
Apprehension
Cyanosis
MANAGEMENT:
Supportive Therapy
Early use of Positive Pressure
Ventilation, reduces ventilator
therapy duration
Avoid aggressive crystalloid therapy
Severe cases may require Ventilator
therapy
EMERGENT TRANSPORT: TRAUMA
Center
CARDIOVASUCLAR TRAUMA:
Any patient with significant
Blunt Trauma or Penetrating
Trauma to Chest has Heart/
Pericardiocentesis
Out of hospital primarily reserved for
Cardiac Arrest
Rapid Transport
IVs of LR/NS
Definitive treatment is
Pericardiocentesis followed by surgery
Pericardial window
Tamponade is Hard to diagnosis
Hypotension is common in chest
injury
Heart sounds difficult to hear
Bulging neck veins may be absent
if Hypovolemia is present
High Index of Suspicion required
Traumatic AORTIC
DISSECTION/RUPTURE:
Caused by:
MVC
Falls from Heights
Crushing Chest Trauma
Animal Kicks
Blunt Chest Trauma
EMERGENT TRANSPORT
TRACHEOBRONICAL RUPTURE:
Uncommon injury
Less than 3% of chest trauma
Occurs with Penetrating trauma or
blunt
High Morbity rate
May involve fracture or upper ribs
Losing air into pleural space
Carina splint common
PATHOPHYSIOLOGY:
Majority (80%) occur near Carina
\Rapid movement of air into the Pleural
Space
Continuous flow of air flow from needle
of decompressed chest
ASSESSEMENT FINDINGS:
Respiratory Distress:
Dyspnea
Tachypnea
Obvious SQ Emphysema
Hemoptysis
Bright Red colour
INTRODUCTION TO CARDIOLOGY:
CARDIOVASCULAR DISEASE:
Single greatest cause of death and
disability in the US
Includes heart disease and Vascular
Disease
2 Million People diagnosed with as
ACS/yr.
1.5 million will experience an Acute MI
Of these 0.5 million will die
ATHEROSCLEROSIS:
Plaque accumulation within the
lumen of the artery resulting in:
Decreased Lumen inner diameter
Increase Vascular resistance
Potential for Thrombus or Embolus
formation
ASSOCIATED WITH:
HTN
STROKE
ANGINA, HEART ATTACK
RENAL FAILURE
RISK FACTOR:
Age
Family History
Hypertension
Hypercholesterolemia
Male
Smoking
Diabetes
CONTRUBTING FACTORS:
Diet
Obesity
Oral Contraceptives
Sedentary Lifestyle
Personality Type
EMS ROLE:
Original was the need for rapid response
to identify emergency care of victims of
Sudden cardiac death (paramedics have
been prove to make difference in survival
and Acute Myocardial Infraction,
Contributions to being reconized in acute
coronary syndromes
Looking for ST Elevation in 3 or more
leads Cardiac Artery is then Splinted or
Stented
Bypass ER Department
PEA- Pulseless
Pulseless V-Tach
Asystoli (Flat line)
Anatomy & Physiology:
When heart must conducts
first
Functionally sypthom
Autocontratility: we can
contract our own
Pulmonary Edema: LCHF:
Conductive SYSTEM:
SA-NODE: (PACEMAKER)
60-100 bpm (RA- Anterior
inferior wall of Atrium)
AV NODE: 40-60 BPM
PERkinjie Fibers: 20-40bpm
Perkinje system
AV JUNCTION- Junctinal
Rhythm
Parietalpericardialsac
Pericardialfluid
Blood Flow:
(Mitral
valve)
CARDIAC CYCLE:
DIASTOLIC
SYSTOLIC
Coronary Circulation:
Usually thought of as 3 arteries
Left (Main) Coronary Artery
Left Circumflex Artery
Left Anterior Descending Artery
Chest Pain
Diaphertic
Pale
Dyspnea
60 and above age
Normtensive-Hypertensive