RESPIRATORY EMERGENCIES

RESPIRATORY EMERGENCIES
o
2000 people
o
Common chief complaint
o
Common in infants and children due to small
respiratory reserve
EMTS plays an important role in the care and transport of
patient with respiratory distress
GOAL OF EMT:
Maintain and improve the patients condition
(perfusion) during transport.
To maintain adequate resp:

Administration of O2

Patient comfort

Assist in inhaler medications

ROLE OF EMT:
Recognize the sign and symptoms of respiratory distress and
intervene
2 Functions of Respiratory System
1. Oxygenation Supplies O2
2. Ventilation Removes CO2
Body Tissues rely on continuous supply of O2 to maintain an
energy producing process called aerobic metabolism
Any interruptions of supply of O2 and removal of CO2 can
quickly lead to biological death.
2 Types of Respiration

External Alveolar / Capillary exchange

Internal Capillary / Cellular exchange

Bronchospasm / Bronchoconstriction
Lower airway are narrowed
Bronchodilator
Dilate Bronchioles
ASSESS DOB (Difficulty of Breathing)

Tripod position (leaning forward, with arms and elbows

locked in front of the pt)

Patients face

Speech

Cyanosis: Peripheral & Central

PHYSICAL EXAMINATION FINDINGS:
Wheezes
o
Wheezing sound upon expiration
Stridor
o
can be heard on upper airway
o
high pitched wheezing sound with Steth
Jugular Vein Distention
o
CHF, Tension Pneumothorax, Cardiac Tamponade
Inspect for Muscle Retraction
o
Asymmetrical chest wall movement

UPPER AIRWAY ADVENTITIOUS SOUNDS: Crowning,

gurgling, snoring, stridor

HYPOXIA
Decreased O2 in cells
Causes:
o
Absence of inadequate respiration (sedation,
morphine overdose)
o
Obstruction of airflow occurring on either
upper of lower portion of respiratory tract.

Pus in alveoli PNEUMONIA

2 Types of Pain
SOMATIC PAIN (e.g appendicitis)

specific/localized

Parietal pain receptors

VISCERAL PAIN (e.g. MI, Chest Pain)

Nonspecific / dull

Visceral pain receptors

COPD (Chronic Obstructive Pulmonary Disease)
Reactive airway disease
Chronic cough or airflow obstruction
2 Includes:
CHRONIC BRONCHITIS
Excess mucus in airway
Destroy the lining of bronchi and bronchioles
PULMONARY EMPHYSEMA
Destroyed / damaged alveoli causing reduction in
lungs surface area.
Decreased O2
BRONCHIAL ASTHMA
Most common in children and young adult
Oversensitive airways to environmental stimuli and
emotional states
Small airways to environmental stimuli and emotional
states
Bronchospasm
Difficulty in expiration
Dyspnea, wheezing, dry cough, over expanded alveoli
DANGER signs of Asthma

Loss of wheezing

Changes in sensorium (confusion, irritability)

Indicating hypoxia if uncorrected may lead to

BRADYCARDIA Cardiac Arrest.
NOTES: Asthma (always consider)
Upper airway obstruction
Pulmonary embolism
Anaphylaxis, bronchial foreign body (Unilateral
Wheezing)
Congestive Heart Failure (Cardiac Asthma)
STATUS ASTHMATICUS
Prolonged asthmatic attack
Widespread mucus plugs
Increased airway resistance
Increased work of breathing
Increased O2 needs
S/Sx: Anxiety, wheezing, overinflated chest, tachycardia,
prefers to sit up and lean forward.
OVERALL AIM: Must be treated rapidly to prevent lethal hypoxia.
HYPERVENTILATION SYNDROME
Abnormal increase in RR & Tidal Volume
Anxiety
Tingling hands and feet
Look for evidence of neck / back injury to r/o traumatic
causes
Abnormal increase in respiratory rate and tidal volume
Ph 7.35-7.45 (normal) if <7.35 ph (acidosis)
Management:
1. Relaxation, slow down breathing
2. Sedation if conscious

3.
4.

Breathing in paper bag no longer advised (can cause

acidosis)
Do not withhold O2 support

RESPIRATORY INFECTION
COPD infant and children
CROUP AND EPIGLOTTIS
CROUP

Viral upper airway

Agitated barking cough
6 months to 3 years of age
Airway obstruction

EPIGLOTITIS

Bacterial infection

Swelling causes airway obstruction

Sits still

Drooling of saliva
PNEUMONIA

Bacteria, virus, fungi

Children / adult

Alveoli and airway filled with pus

Decreased O2
PULMONARY EDEMA

Fluid accumulation in the lungs

Due to CHF / MI

Inhalation of smoke and toxin fumes

High altitude, narcotic overdose, fluid overload

S/SX:
Cyanosis, crackles, distended neck veins, pinkish
frothy sputum, peripheral edema Swelling of
extremities
Management:
High Flow O2
Consider PEEP/CPAP
Transport immediately
PULMONARY EMBOLISM

Clot/embolus that blocks a pulmonary artery

Blood cut in DVT (deep vein thrombosis) beaks off

and travels to lungs interrupting blood flow to a lung
portion

Usually post-operative / bedridden pts.

Dyspneic and Tachycardia

Transport to hospital immediately with O2 support.

PNEUMOTHORAX / HEMOTHORAX

Blood/air in the pleural cavity causing collapse of

lung parenchyma

Associated with chest pain and tachypnea

Decreased breath sounds

CHIEF COMPLAINT
1. How long has it been present
2. Was the onset gradual or abrupt
3. Is the dyspnea made better or worse
by any particular position
4. Has the patient been coughing
5. Is the cough productive?
What does the sputum look like
6. Is there any associated Pain
7. Past Medical History
8. Medications

Indication of a patient in a reclining/supine position

Mild respi distress

Severe respi distress too exhausted

Pts. Face

Pts. Speech
Pts. Skin and mucus membrane

O nset
P rovocation
Q uality
R adiation
S everity
T ime
GEN IMPRESSION IN RESPIRATORY DISTRESS
Patients mental status
Restless, agitation, unresponsive
Patients position (Tripods)
Sit upright and leaning forward

CARDIOVASCULAR
EMERGENCIES

O nset
P rovoKE
Q uality
R adiation
S everity
T iming
A ssociated Symptoms

EMS AND DISPATCH

Trained to recognize symptoms even if atypical
Provide pre-arrival notification
Monitor and cardiac rhythm, be prepare to provide CPR
Time and onset of symptoms to stabilize, triage and
transport pt.
MI 6 hours
ER They are counting the onset of pain
2010 Recommendation All Dispatchers should be appropriately
trained to provide telephone CPR (Class I)
To help bystanders recognize cardiac arrest, dispatchers should
inquire about:
Absence of consciousness and Quality of breathing
Recommended CPR for unresponsive who are not breathing
normally
Most are cardiac arrest
Frequency of serious injury from CC in the non-arrest
graoup is very low
Instruct untrained Lay rescuer to provide CPR for adults
with SCA (Class I)
Include Rescue breathing instructions if adult/child with
a high likelihood of asphyxial cause.
ACUTE

CORONARY SYNDROME
Witness arrest in ventricular fibrillation (VF)
90 % cause of death
EMS dispatch personnel should be trained to respond

ANGINA PECTORIS (CHEST PAIN)

Presenting sign of acute MI, portion of myocardium is
not receiving enough oxygenated blood
Risk factors:

Sedentary lifestyle

Cigarette smoking

Obesity

High in cholesterol

DM

Male

Age >50

HTN >140/90

Family Hx of CHD

Oral contraceptive >40 y/o pills-(viscous blood)

Angina Pectoris
Acute Coronary Syndrome
MI
Signs and Symptoms:
o
Mistaken for indigestion
o
Chest pain after exertion/stress
o
Relieved after administration of Nitroglycerin
o
SOB, Nausea, increased PR
NITROGLYCERIN VASODILATE CORONARY
ARTERIES
Sign that it is improving = Headache
Contraindication:
Right ventricular infarcation
Initial systolic BP of 90mmHg within 24 hours
PDE (Tadalafil) 5 Inhibitor (48 Hours)
Emergency Care:
1. Chew on aspirin (160-325mg) 4 tabs
Indication: bleeding and allergy
2. Find out if the patient is: taking Nitroglycerin, last
dose taken, how much was taken.
3. EMS may administer O2 at 1 rate as soon as
possible
4. Contact EMS: Inform the patients condition
5. Nitroglycerin tab/spray (3-5mm) with permission if
the diastolic BP is above 90
6. Emotional support
7. Continue to monitor V/S
NITRATES: (Nitroglycerine)
ISORDIL
Dinitrate, fast acting, short duration
INDUR
Mononitrate, Slow acting, for
maintenance
ACUTE MYOCARDIAL INFARCTION
o
Portion of myocardium dies (necrosis)
o
Due to deprived coronary blood flow
Signs and symptoms:
Chest pain related to stress and exertion
Pain originate from the sternum
Sharp, squeezing or throbbing pain
Pain lasts 30 minutes hours
15-20% are painless Silent MI attack
Not relieved by NTG (Nitroglycerin)
Respiratory: Dyspnea, cough with sputum
production
Behavioral: Impending doom, Anxiety, Irritability,
Depression, Mild delirium
Circulatory: Pallor, Diaphoresis(excessive
sweating), decreased BP
Complications:
Cardiac Arrest 40%
CHF
Shock (24hours) Cardiogenic
Pulmonary Edema
Cardiac Dysrhythmias
CORONARY ARTERY OCCLUSION
Ischemia
min after occlusion
Necrosis
5-6 hours
Healing
5-6 Days
Scarring
12 days
Maximum
6 weeks
Emergency care MI
A. Conscious Patient
- High conc. Of O2
- Keep calm and still
- take HX and determine s/sx
- Help with prescribed medication

B.

Semi sitting position Provide quiet transport

Out of Hosp. ECG determine: Unstable Angina,
STEMI, NTEMI
Unconscious Patient
- Maintain Airway
- CPR / Defrib if needed
- O2 via BVM
- Quiet transport
- Monitor V/S throughout care and transport
A aspirin
M orphine
O xygen
N itrates
MI
Pain r/t stress
Not relieved by rest
rest
NTG may relieved pain
Reduced BP/Normal
Diaphoresis

Angina
pain follows stress
Pain relieved by
Relived by NTG (if not
(3 doses in 10 mins-AMI)
Not affected
Short term diaphoresis

AORTIC ANEURISM
Outpouching of BV
Abdominal aortic Aneurysm
80% mortality if hypotensive
S/sx:
Ripping, tearing and sharp pain that starts at
the back between shoulder blades
Syncope with back pain or hypotension
BP discrepancy bet. Arm/decrease in femoral
/carotid pulse
RISK FACTORS ANEURYSM
Men >60
Smoker
Family HX
Obesity
High cholesterol level
CLASSIC TRIAD OF ANEURYSM

Abdominal pain

Hypotension

Pulsativemidabdominal Mass
Signs and Symptoms
Abdominal tenderness
Bruit over aorta
Palpable Mass (Not effective in obese)
Rate of Expansion:
4-4.9
3.3% rupture
5cm
14%
75cm
20-40% risk of rupture
18% - survive
EMERGENCY CARE FOR ANEURYSM

Calm and reassure the patient

Administer 100% O2 by NRM

Place in comfortable position

Transport without delay

HYPERTENSIVE EMERGENCIES
- HTN with >140/90
- Renal damage
- Heart failure
- Hypertensive retinopathy
- Brain stroke
HYPERTENSIVE CRISIS
No organ end damage
Increased BP
EMERGENCY: END ORGAN DAMAGE
Signs and Symptoms:

 Severe headache
Nausea and Vomiting
Altered Mental Status
Aphasia, Sudden blindness
Muscle twitching
Seizures
Hemiparesis
EMERGENCY CARE:
Secure airway, administer O2
Transport without delay
Be prepared to deal with seizures
CARDIAC TAMPONADE
Accumulation of blood in the pericardial sac
Stab wound to the heart and acute MI with cardiac
rupture may cause the myocardium to fill with blood.
Signs and Symptoms
Decreased preload because of fibrous tissues
Cannot fill the heart\muffled heart sounds
Decreased BP
Distended neck vein
Pale, cool, sweaty skin
Tachycardia
EMERGENCY CARE
Place the pt. in a semi-fowlers position. Administer O2
Immediate transport
Monitor en route to the hospital (trauma surgeons may do
immediate pericardiocentesis)
IRREVERSIBLE DEATH
o
Rigor
o
Lividity
o
Decomposition
o
Injuries not compatible to life
PERICARDITIS
Inflammation to pericardium
Idiopathic infection and metabolic factors as well as
trauma and tumor
Signs and symptoms

Dyspnea

pre-cardial pain aggravated while breathing

fever, chills, fatigue (infection)

EMERGENCY CARE
ABC
Administer O2 NRM
Immediate transport in sitting position
Monitor pt. enroute to the hospital
CONGESTIVE HEART FAILURE
Excessive fluid buildup on the lungs; inadequate
pumping
Signs and symptoms:

Tachycardia, Dyspnea

Pulmonary Edema with rales

Frothy white/pink sputum

Normal / increased BP

Cyanosis

Pedal Edema

Engorged neck veins(late signs)

Enlarged live, spleen with abdominal distention (late

sign)
Stroke volume = 60-70ml
Preload 70
Defective 69
1ml-intravascular space
Left sided lungs
Right sided pulmonary edema
Paroxysmal Nocturnal Mild dyspnea

Can sleep but will wake up complaining dyspnea

EMERGENCY CARE
Semi Fowlers/sitting
Increase O2 through NRM
V/S throughout care and transport
CARDIAC PACEMAKER
>40 bradycardia
Heartblock
Will not present AMI, Angina Pectoris and CHF
Care same with persons pacemaker
Usually placed below the clavicle, is visible and can be
palpated
Signs of Pacemaker malfunction

Slow and irregular pulse

Signs of shock

Pt. complaints of chest pain

Pacemaker battery - NO DEFIBRILATE
IMPLANTED DEFIBRILLATOR
When patient develop VF, it identifies the rhythm and
shock the patient.
EMERGENCY CARE AND CPR

Patient are the same for other cardiac patients.

CARDIAC BYPASS SURGERY
Restore blood flow to a section of the myocardium
Patient should tell you he had a bypass surgery
Observe for a midline surgical scar on chest of an
unconscious patient
OPEN HEART Direct cardiac massage
RESTERNOTOMY Should be done on an
appropriate equipped ICU / operating suite
BROGADA SYNDROME sudden VFib

NEUROLOGICAL DISORDERS
SEIZURE

Electrical activity of brain become irregular

Not a disease but rather a sign of an underlying disease

Common causes of seizure
Hypoxia
- Hypolycemia
Infection
- Trauma
Poisoning
- Impaired Cerebral
Oxygenation
Overdose
- Epilepsy uncontrolled meds
Intoxication
- Brain Tumor
Idiopathic
Types

Partial

Generalized
FEBRILE SEIZURE

Generalized tonic-C-P

2-5% of the dse

Self-limiting

6mos-6yrs

No medication

Middle ear problem

STATUS EPILEPTICUS

Generalized T-C-P

Associated risks
Life threatening
Continuous

ASSESSMENT
Scene size up
1. Be alert to the threats
2. Focus on any possible indication of trauma
3. Determine the need for additional resources
4. If the pt. is still seizing upon arrival position the pt. and
objects around him in a safe manner

TRANSIENT ISCHEMIC ATTACK

Recurrent neurological deficit
Weakness, paralysis, speech disturbances
Few secs 12 hours
Disorientation of cerebral artery and basilar artery
Signs and Symptoms
Hemiparesis
Unilateral Numbness
Aphasia
Slurred Speech
Vertigo
Convulsion
2 Main Types of Stroke

Ischemic

Hemorrhagic

1. Maintain Airway and ventilator concern

2. High flow of O2 and utilize pulse Dx
3. Support breathing Initial Assessment
4. Evaluate the quality of circulation
5. Determine priority status
Focused History and Examination
1. Complete rapid assessment, VS, rapid transport
2. SAMPLE history from relatives if unresponsive
3. Assess head and neck
4. Equality of pupils
5. Test B G L if hypoglycemia Is present / suspected
PARTIAL SEIZURES
A. Simple Partial
Focal motor / focal sensory
Jacksonian March
AURA: Small bright lights, rising sensation to
stomach
Patient usually awake
Tingling, stiffening or jerking in one part of the body
B. Complex Partial
Psychomotor
Abnormal behavior
Glassy stare, lip smacking or chewing
Fidgeting with clothing
Temporal lobe seizure
1-2 mins
GENERALIZED SEIZURES
A. T-C-P / GRANDMAL
Tonic - rigid stiffening ; 30 secs
Patient might bite his tongue
Breathing may stop
Clonic - Jerks violently ; 1-2 mins
Foaming and drolling
Inefficient breathing-cyanosis
Post Ictal - Recovery; 5-30 mins
State of drowsiness
Deep sleep
Regain consciousness
B. Petitmal / Absence

Blank Stare; 1-10 secs

Children

No dramatic motor activity

GRANDMAL SEIZURE
Stages: AURA TONIC CLONIC POSTICTAL
EMERGENCY CARE
1. Position
2. Maintain patent airway
3. Assess Breathing
4. O2
5. Prevent injury
6. Appropriate transport
ONGOING ASSESSMENT

Be prepared to manage additional S/SX

Monitor CAB

Repeat and record VS

Document
H.O

Protect the patient from injury and guard his

airway but never put anything hard on his mouth
Do not restrain. Remove objects from his path
Loosen obstructive clothing

STROKE / CVA
Cause by non-traumatic brain injury resulting in
occlusion/rupture of cerebral blood vessel.
Classic Signs and Symptoms of Stroke
1. Confusion/Disturbed Mental Status
2. Facial Droop
3. Seizure
4. Inappropriate behavior pattern
5. Dysarthria, Aphasia
6. Irregular Pulse
7. Stiff Neck
8. Hemiparesis
9. Hemiplegia
10. HPN
11. Staggering gait/Incoordination
Risk Factors CVA
Cannot change / Non Modifiable

Age

Race: African, American, Hispanic

Men: 75, Women- More fatalities

Family History

Prior History of Stroke/TIA

Can be change / Modifiable

HPN imp factor after age

DM, High Cholesterol

Clot formation

Peripheral vascular dse, hemophilia, syphilis

Smoking, Physical Activity, Obesity

Use of Birth Control Pill, blood thinner

Alcohol

Street Drugs, such as cocaine

General Sign and Symptoms
Loss of consciousness
Arm drift
Drooping face
Paralysis
Unequal size of pupil
Common findings
Facial drooping
Abnormal arm drift
Speech Disturbance
ISCHEMIC

Lifestyle causing; 80-85%

Blockage in arteries supplying O2 blood, and blood

supply

Narrowing lumen; fat deposition

HEMORRHAGIC

15-20%


Rupture and weakening
2 main causes
Associated with HPN
Aneurysm which balloons out, weakening and thinning
until it ruptures
Arteriovenous malformation AVM cluster of enlarged
and structurally weak blood vessels

Cocaine seizure and stroke

UNDERDOSE/UREMIA
Noncompliance, med. Seizure
Diabetic coma
COPD, Uremia (toxin build up)
TRAUMA/TUMORS/TEMP
Trauma direct damage
Tumor increase ICP
Temp extremes impact on consciousness
INSULIN
IDDM
Hypoglycemia
PSYCHOSIS
Schizo, Manic Depressive
Delirium Memory loss
Lithium (Eskalith, Lithobid)
Risperidone, Olazapine
POISONING
Carbon Monoxide prevent O2 reaching the brain
Overdose of tricyclic anti-depressant (hypotension and
dysrhythmia)
STROKE/SHOCK
Massive strokes cause coma
TIA Mini strokes (subsides within 24 hours)

PREHOSPITAL TREATMENT OF STROKE

LOAD AND GO

As there is a three hour window of opportunity for the

initiation of thrombolytic therapy in case of Ischemic
Stroke
1. BSI, safety
2. Can protect patent airway do not interfere
3. No gag reflex left lateral position with head slightly
raised
4. Administer O2 gently if required
5. Ventilate when necessary ETCO2
6. VS
7. Monitor Cardiac Rhythm set
8. Beep tone monitor for Bradycardia& PVCs
9. Protect paralyzed extremities
10. Provide comfort and honest reassurance

ASSESSMENT AND CARE

Unknown history of AMS
SCENE SIZE UP
Use clues if trauma/medical
Medication found number of patients

Role of EMS in STROKE CARE

Rapid activation of EMS
7 Ds of stroke management
1. Detection recognize
2. Dispatch prioritize call
3. Delivery Transport to stroke center
4. Door hospital; provide thrombolytic within one hour
5. Data CT Scan
6. Decision Fibrinolytic Therapy; Identification
7. Drug Treatment

INITIAL ASSESSMENT
Manual C-spine immobilization precaution
CAB
Establish Priority
Guidelines
Change in Mental status
Airway discrepancy
Breathing inadequacy
Circulatory deficit
FOCUSED HISTORY AND P.E

SAMPLE

V/S

PE Rapid M. exam, Focused M. Exam

Types of CEREBRAL EDEMA

Cytotoxic

Vasogenic

Interstitial
Management
Fluid Restriction
Elevate the head 20-30 degrees
Oxygenation and Ventilation
Agitation and Pain control

EMERGENCY MED. CARE

Maintain stabilization

Patent airway

Increase flow of O2; assist on ventilation

Position

Transport

ALTERED MENTAL STATUS

Change in normal mentation
A lcohol and other drugs
E pilepsy, Endocrine, Exocrine
I nsulin (Hypo, Hyperglycemia)
O xygen, Overdose, Opiates
U remia/Underdose
T rauma/ Temp/Tumor
I nfection
P oison and psychiatric
S hock, stroke or space occupying lesion

Classification of Stroke
1. TIA
2. Reversible Ischemic Neurologic Deficit
3. Completed Stroke / Stroke in evolution

ACIDOSIS
Diabetes, shock, poisoning, kidney failure
ALCOHOL
Inhibits brain, impaired judgement
Cannot maintain airway
Aspirating saliva/vomitus
EPILEPSY
Excessive discharge of electricity
Alcohol withdrawal
INFECTION
Increased temperature, inflammation
Meningitis, encephalitis, altered LOC
OVERDOSE
Barbiturates and Narcotics suppress (Heroin)
Narcotic slows down RR

Types of CVA by Etiology

Ischemic
Thrombosis
Embolism
Hemorrhagic
Intracerebral
Subarachnoid
HEMORRHAGIC
Seizure more common
Increase ICP Hemorrhagic
Risk of stroke increases with age
Increase BP Rebleeding tendencies
Do not treat if theres HTN/HPN
Rapid Transport
Causes: Brain tumor, Anticoagulant therapy, Cocaine, HPN

ISCHEMIC
Tissue plasminogen activator
Calcium channel blockers
Prevent ischemic cascade
Delay: Sleeping
Unable to recognize

EMERGENCY CARE
HYPOGLY/HYPERGLYCEMIA
EMERGENCY CARE OF HYPERGLYCEMIA
Increase concentration of O2 at 15 LPM by NRM
Immediately transport to medical facility
Arrange for ALS intercept
Complications:
o
Retinopathy Blindness
o
Neuropathy Damaged nerves, septicemia
o
Nephropathy Damaged Glomeruli
Long term:
1. MI Develop thrombus, dislodge in coronary
arteries
2. CV
3. Pulmonary Embolism
4. Impotence

HYPOGLYCEMIA
Causes:

Has taken too much insulin

Not eaten

Over-exercise

Vomited a meal
Sign and Symptoms:
Rapid Onset (mins)
Drooling saliva
Hunger
Fainting, occasional coma
Odorless Breath
Cold Clammy skin; profuse persp[iration
Normal BP
Eyes normal
Decreased LOC, altered Mental Status
Hostile behavior appear to be acute alcoholic intoxication
EMERGENCY CARE
Conscious, Hypoxic
Breathing device Semifowlers
Pulse Ox if connected
Lateral recumbent position (with breathing)
Provide O2
Transport
ALS Intercept
THINGS TO REMEMBER:

Do not give insulin hypoglycemia

Direction should be always hypoglycemic

Direct care to hypoglycemia

Look for medications, info card, insulin in refrigerator

r/o hypoglycemia assume that it is hypoglycemia give

sugar

SAFETY
- Patient should be conscious
- Able to swallow
- Should not be hypoxic
Avoid: coke zero, 7up

Give
sugar

ONGOING ASSESSMENT CVA

Continue to monitor pts status
Provide other treatment
Repeat and record V/S: every 5 mins (unstable) every 15 mins
(stable)
HYPERGLYCEMIA AND HYPOGLYCEMIA

Homeostasis normal BGL 70-110 mg/dl or 80-120 mg/dl

Increased Blood Glucose Level

Beta cells will release insulin

Increased rate of glucose transport into cells

Increased utilization of glucose and ATP

Increased conversion of glucose to glycogen

Increased protein synthesis

Increased fat synthesis

Result: BGL Declines
Increased Blood Glucose Level

Increased breakdown of glycogen to glucose

Increased breakdown of fats to fatty acids

Increased synthesis and release of glucose

Result: BGL Rises
NIDDM (TYPE II)
Pancreas is still able to secrete insulin but not enough
IDDM (TYPE I)
Pancreas secretes little or no insulin
HYPERGLYCEMIA
3 Ps
Polyphagia
Polydipsia
Polyuria
Causes
Not diagnosed/treated
Has not taken his insulin
Overeaten, too much Carbohydrates
Suffers an infection which affects glucose
Signs and Symptoms:
Gradual (Takes time, days)
Dry mouth, intense thirst
Abd. Pain
Gradual increase in restlessness followed by coma
Weak, rapid pulse
Kussmauls respiration deep, hyperventilation
Acetone- sickly sweet children
Normal/Slightly High BP
Sunken eyes
Hostile/aggressive behavior
Loss of elasticity (Farrod tongue)
Hyponatremia and hypokalemia
Brain cells does not require insulin
Myocardial and Skeletal Muscles needs insulin
Question to be asked:

Have you taken your hypoglycemic meds?

Have injected yourself with insulin: check for

needle marks

Did you vomit when you have eaten

Did you undergone strenuous activity aside

from your routine
Things to Prepare:
1. PPE
2. Circulation
Meds:

Glucogel Cheek

Table sugar under the tongue

Insulin not given by EMT

3. Airway

OPA, NPA, SALT

Suctioning device
4. Breathing

Pulse Oximeter

If hypoxic do not give GLUCOSE

NRM

Supplemental O2

IV Fluids PNSS given by paramedics

TYPE I
-

Hyperinsulinemia
Hypoglycemia
Insulinsia

Type 2 (Oral hypoglycemic, diabetic diet)

Hyperglycemia
Hypoinsulinemia
Ketoacidosis/Diabetic Coma

HEAT AND COLD EMERGENCIES

TEMPERATURE
Heat produce and heat loss
Measured in Celcius
Temperature Control
Core Deep tissues of the body
Essential for metabolism
Peripheral
Surface; not critical
Skin, fats
Skull, vertebral column, chest abdomen, pelvis
Method of getting Temp
1. Rectal accurate, high and low temp
2. Oral less than rectal; altered by fluids
3. Axillary 4. Tymphanic Correct positioning forehead
Temperature Regulation
Hypothalamus thirst center, hunger. Body temp regulation,
ANS
Skin Cold and warm receptor
Factors affecting temperature:
1. Environmental condition
2. Physical condition (Female hormones, exercise, dse)
3. Alcohol, drugs and medications
4. Age (infant, children, elderly)
5. Nutrition / Hydration: Dehydration, Malnutrition
How the body keeps warm
- Constricting peripheral vessels
- Limiting perspiration
- Increasing metabolism
- Shivering
- Erecting hair on the skin
HEAT PRODUCTION

Metabolism

Endocrine

Shivering

Muscular activity

External heat sources

MECHANISM OF HEAT LOSS
1. Conduction two touching objects
2. Convection air and electric current (e.g fan)
3. Radiation without direct contact (e.g sun)
4. Evaporation water to gas
5. Breathing and respiration
COLD EMERGENCIES
HYPOTHERMIA
Looses more heat than it gains
2 Main types
Gen Cold Emergency (GENERALIZED HYPOTHERMIA)
Whole body
Life threatening
LOCAL COLD INJURY (Peripheral C.I)
- Specific area(e.g frost bite)
Factors that contribute to hypothermia
Cold windy environment

Drugs/alcohol intake
Alzheimers dse
Previous cold exposure
Use of drugs/alcohol
Low blood sugar
Very young less fats
Elderly Poor diet; loss of fats, delayed circulation
ILLNESS AND INJURIES THAT CONTRIBUTE TO
HYPOTHERMIA

Shock

Head and Spinal injuries

Burns
Sepsis Low BSL
3 STAGES

Mild 34-27 C or 96-93.2 F

Moderate 30-33 C or 86 F

Severe less than 30 C

MILD HYPOTHERMIA
High HR and RR
Cool Skin; Shivering
Joint Aches
Slurred Speech
Difficulty of moving
MODERATE HYPOTHERMIA
Shiver decreasing
Rigid muscles
Low HR and RR
Pale, blue, mottled skin
Dilated pupils
BP unappreciated
SEVERE HYPOTHERMIA
Unresponsive
Rigid muscles
Blue skin
Slow/absent respiration
HR slow
PR hard to feel
Cardiac Arrest
HISTORY TAKING

SAMPLE history

If unresponsive:
Alcohol abuse
Thyroid disorder
DM
Stroke
Trauma

Also ask for:

How long pt is exposed
Source of cold
Activities before symptoms began
GENERAL PRINCIPLE EMERGENCY CARE (HYPOTHERMIA)
1. Remove from cold envt.
2. Remove wet clothing, cover with blanket
3. Avoid rough handling
4. O2 should be warmed and humidified (100 %
5. Via NRM)
6. Avoid stimulants
7. Do not massage extremities
8. Check pulse 30-45 secs
9. Before BLS, CPR is only successful when patient is
rewarmed
10. Document.
2 Types of REWARMING
PASSIVE
No use of heat

Warm environment
Applying blanket

ACTIVE
Direct application of heat
Contact med protocol first
Application:
Mild hypo active rewarming
Warm blankets, heat pads
Place dressing bet heat packs and skin to avoid
burn
Moderate hypo heat pack to torso
Avoid underlying tissues
Severe Hypo Active
Warm blanket
Done in the hospital
LOCAL COLD INJURY
Ears, nose cheecks, chin, feet
Risk LCI
DM Alcohol
Nicotine
Heart Disease

Classification:
A. Superficial Cold Injury (Frost nip)
Upper layer
Gray and White
May not be seen immediately
Stinging sensation
Numbness
B. Frost Bite (Late)
Deep Cold Injury
Waxy appearance
1-7 days blisters
Gangrene may set in
Burning and throbbing pain
EMERGENCY CARE DEEP FROST BITE
1. Safety BSI
2. Give O2
3. Remove jewelry before swelling
4. Splint the injured extremities
5. Avoid Breaking Blisters, applying heat, walking
6. Submerge in a warm bath 37.8-40.6 C
7. Use sterile gauze / cotton to separate the frostbitten
fingers and toes.
8. Continue until the tissue is soft
9. Enroute
10. Assessment
11. Document
EMERGENCY CARE FOR EXTREME COLD
1. Remove wet clothing
2. During transport, rewarm the patient
3. Provide care- CAB
4. Warm fluids for conscious and alert
5. Keep the pt. at rest
HEAT EMERGENCIES
HYPERTHERMIA
High core body temp.
Produce more heat that it looses
HEAT RELATED EMERGENCIES

Heat Cramps

Heat Exhaustion

Heat Stroke

HEAT CRAMPS
Strenuous activity
Electrolytes and H2O loss
Painful spasm shoulders, arms, abdomen
It may appear the pt. is having acute abd. Pain
Sodium loss
EMERGENCY CARE:
1. Move to a nearby cool place
2. Fluids- conscious patient
3. Massage cramped muscle
4. Apply moist towels to pts. forehead
5. Rest, transport
HEAT EXHAUSTION
Too much heat and dehydration
Sign and symptoms:
Sweating
Signs and Symptoms:

High HR

Normal/Subnormal BP

Fainting

Cold clammy skin

Rapid, shallow breathing

Weak pulse
EMERGENCY CARE FOR HEAT EXHAUSTION
1. Cool Environment
2. Remove excess clothing
3. Drink Water
4. If Severe: IV Fluids (ALS)
HEAT STROKE
No Sweat
Load and go
Body cooling system shut down
Risk:

Athletes
Fire fighters
Military recruit
Construction workers

Sign and symptom

Altered m.s

Dry hot, flushed skin

>39.4C

Low HR

Shallow, deep breath

Muscle twitching

Dilated pupils

Unresponsive
EMERGENCY CARE FOR HEAT STROKE
1. Med. Direction
2. Call ALS transport stat
3. O2 PPV / Supplemental
4. Start cooling
5. Remove outer clothing
6. Cool pack neck, groin, armpit
7. Comfort
8. Ongoing assessment
9. Document

Environmental ( Insect Bites

and Stings )

Toxins produced by animals/plants

Arthropods
Reptiles
Venomous Marine Life

50% insects
30% snakes
14% spiders
Hymenoptera
Bees, hornets, wasps, fire ants
Local pain, mild redness, swelling, itching, toxic venom
Local effect
Edema
Systemic
Urticarial, flushing, Itching, mild UA Obstruction,
laryngeal edema, hypotension, severe bronchospasm

Pam, swelling

30 mins to hour

Rapid pulse and labored breathing

Blurring vision

Nausea and vomiting

Drowsiness & unconsciousness

Bite on skin
Management:

Calm

02

Locate fang marks clean soap & H20

Remove jewelry from bitten extremity

Keep bitten extremity immobilized

Watch band for edema

Apply contracting band above and below

Transport
Do not:

Apply ice
Tourniquet
Cut & suck
Electric shock
Locate snake

Venomous Marine Life

Jellyfish - vinegar/alcohol, burning pain
Sting ray Flush, hot water, elevate, cover
Sea urchin immersed on hot H20, vinegar, large spine dont
remove
Dog and Cat bites
Most commonly bitten
1. Head
2. Neck
3. Upper Extremities
Face - 11 %
Trunk - 7%
Upper E - 28%
Lower E - 31 %
* Under 12 yrs. old face
* dog bites occurs in hot weather
Dog Bite 450psi
Crushing type injuries
Cat Bite sharper teeth
Punctured wound
Emergency Care
Circulation:
Control bleeding
Direct pressure and cover
Wash wound
Removed jewelries

Airway:
-

Airway
100% 02
High risk for wound infection- transport
Ongoing assessment

Emergency Care

Airway

02 100%

Scrape & credit card

Avoid using tweezers

Remove jewelries

Transport
Anaphylaxis Management

Remove stinger

Airway

02

Shock position trendelenberg

EPI auto injector

ALS back up
EPI Auto Injector
Site: vastuslateralis fast absorption
Action: bronchodilate, relaxes airways
Indication:
s/sx of anaphylaxis
prescribed
authorized by med-direction
contraindication
life threatening
2 types
Adult Epi - .3mg (66lbs)
Junior Epi - .15mg (33-66lbs)
*Can be administered twice
Procedure:

Expose

Remove safety cap

90 degress lateral thigh

02 first

Monitor VS
Side effects:
Nausea & Vomiting
Headache
Dizziness
High RR
Anxiety
SPIDER ( black widow, brown recluse )

Neuro toxic

Local cold application

Anti-venom

Padded splint
SCORPIONS
Lethal in children
S/sx: SLUDGEM
S- Salivatism
L- Lacrimation
U- Urination
D- Diarrhea
G- Gastric Cramps
E- Emesis (vomiting)
M- Miosis (pupil constriction)

Snake(Rattle Snake, Copper head, Coral Snakes -Death

occur from respiratory after 36 hours)

Red and Yellow kill

Red or black venom lack

-

Air embolism
Rupture of teeth

Rupture of eardrums

MAJOR CAUSES OF WATER

RELATED EMERGENCY
MAJOR
1.
2.
3.
4.
5.
6.
7.
8.

CAUSES OF WATER RELATED EMERGENCY

Getting exhausted in water
Losing control and getting swept
Losing support
Getting trapped or entangled while in water
Using drugs or alcohol before getting in the water
Suffering hypothermia
Suffering trauma
Having a diving incident

DROWNING ACCIDENTS PREVENTION

(3 warnings)

Children should be under constant supervision if pool is

nearby

Water sports and alcoholic beverages should never mix

Life preserves / life jackets should always be worn when

boating
STAGE
-

OF WATER RESCUE
Reach and pull
Throw
Tow
Go

STAGES OF MANAGEMENT OF DROWNING

1. Do not enter water unless trained in water rescue
2. Ensure open airway and attempt rescue breathing
3. Check pulse, if no pulse, cstart CPR
4. Transport
5. PEEP to dry lungs!
PATHOPHYSIOLOGY
Water enters airway enters the larynx(laryngospasm)
hypoxic triggers airway resistance stiff lung HYPOXIC DRIVE
stimulate inhalation of water with air and chemical FROTH
formation = Brain damage
BAROTRAUMA
Injury to air spaces
Injuries from Baro of Ascent
1. POPS (PULMONARY OVER-PRESSURIZATION SYNDROME)
Burst Lung Hyperbaric Chamber
recompression
6ft to rupture alveoli
Avoid giving PEEP
What to find out about diving accident

Type of diving

Diving activity

Site of diving

Number of dives (72 hours)

Details of in-water recompression

Dive complications

Pre-dive and post-dive activities

Onset of symptoms
INJURIES FROM BAROTRAUMA OF DESCENT
Ear Squeeze
Rupture of tympanic
Middle ear squeeze
Diving with URTI
Descent and ascent
Internal ear squeeze
Forced valsava maneuver

Roaring tinnitus
Sinus squeeze
Does not equalize in frontal and maxillary sinus
ARTERIAL AIR EMBOLISM

Breath holding during ascent

Life threatening

10 mins. Altered consciousness

Visual disturbances

Unequal pupils
MANAGEMENT
1. CAB
2. 100% O2
3. Left lateral recumbent
4. Ventilation ETCO2
5. Decompression chamber
6. Steroid of prescribed
7. Diazepam, dopamine
POPS
-

compressed air in the lungs Lung tissue ruptures

Result:
-

Pneumothorax
Pneumomediastinum
Subcutaneous Empty
Arterial Air embolism

Sign and Symptoms:

Respiratory distress

Substernal chest pain

Diminished breath sounds

Hemoptysis

TREATMENT:
Rest
O2
Reduce size of bubbles no PEEP
DECOMPRESSION SICKNESS
Gas trapped deep in the body tissues
Slow circulated tissues

POISONING EMERGENCIES

INJURIES IN DCS
A. Cutaneous bend / Skin bend

Pruritus, scarlatiniform, mottled rashes

Result from lymphatic movement

Peau d orange localized swelling

B.

Musculoskeletal bends / Joint bends

Deep dull ache
Movement worsen pain
Inflating BP cuff over area relieves pain

Central Nervous system DCS

Brain involvement; deadly
CVA, paresthesia, paralysis

Pulmonary / Chokes
Chest pain, cough, dyspnea
Pulmo edema (pinkish frothy sputum)

C.

D.

DCS MANAGEMENT:
1. CAB
2. 100% O2 Haldane effect (Helps wash out Nitrogen in
the lungs)
- Ventilation ETCO2
3. IV with LR(Lactated Ringers)
4. Lateral Recumbent if air embolism suspected

5.
6.

Transport to recompression chamber

Steroids on med. Control

NITROGEN NARCOSIS THE NATES

Ruptures of deep
Pressurized nitrogen toxic effects on CNS
Anesthetic effect due to lipid solubility of
N2(intoxication)
70-100 feet dives
Sign and Symptoms:

Euphoria

Confusion

Disorientation

Slow motor response

TREATMENT:

Surfacing correct problems

Consider CO2 toxicity

HOT COMPRESS
Breakdown enzymes
Dilute the toxins
AMBULANCE EQUIPMENT

High visibility vest

Ambulance trolley cat

Folding secondary trolley cat

Basket rescue stretcher

Stair chair

EVAC stair chair

Vacuum mattress

Portable suction unit

Hand powered suction unit

ATV

Deep valves- Green >10cmHg Orange > 20cmHg

ResQ Pod

Air splints

Prosplints

Sam splint

Sager femoral traction splint

Portable Doppler

Glucometer
FATAL AMBULANCE CRASHES
Striking vehicle
Travelling in emergency mode
Crash on intersection
Poor driving history

POISON
Solid/liquid/gas
May be swallowed, inhaled, absorbed, instilled
TOXINS
Poisonous subs, secreted by bacteria, plants
ANTIDOTE
Neutralizes poison
3 LEADING CAUSES OF POISONING
1. Alcoholic intoxication
2. Metamphetamine (shabu)
3. Isoniazid (INH) toxicity (hepatotoxic, neuropathy)
CLASSIFICATION OF POISONING
1. Ingested (common route)
2. Inhaled (quickly absorbed)
3. Absorbed
4. Injected
5.
National Poison Management and Control Center
2 types of poisoning

1.
2.

Accidental/unintentional
People mistake poison for food/drink because it is not in
its original container
People misuse chemical product
Misuse pesticides
Young children
Self-poisoning/parasuicide/intentional
Acute exposure
Single contact
Lasts for seconds/ hours
Chronic Exposure
Months, years
May not cause sign and symptoms of poisoning
at first

COMMONLY ABUSED /MISUSED

Stimulants
Depressants
Hallucinogens
Designers drugs
ACTIVATED CHARCOAL 60%
Fine, odorless, black and tasteless powder made of
wood
Acids and alkaloids
Aspirin, amphetamines
No authorization
Unable to swallow
Altered mental status
Contraindicated:
iron, lithium, potassium and ethanol
Brand Name : Liqui Char, super char, actidose 1gm/kg
Dosage
Adult 25-50g
Child 12.5-25g
Infant (up to 1 year) 10-25g
INCOMPABILITY: Syrup of IPECAC
Special considerations
Order from med. Direction
Right patient
Harmful/fatal
Drink through a straw
Do not mix with ice cream
Reassess CAB
Watch out for vomiting
Ongoing assess every 5 mins
Decreasing mental status Sings of worsening condition
SYRUP OF IPECAC
From plant
Indication
Induce vomiting
Conscious patient
Action:
Empties the stomach
Contraindication:

Stupor/coma

No gag reflex

Acute MI

Ingestion of corrosives (strong acids)

Hydrocarbons

Seizure

Pregnant

<6mons

iodides
Effects
may cause heart problems
Special consideration

Pt should be encouraged to WALK after taking the

syrup

Avoid getting this syrup to pt with eating disorder

Not be given with AC


Be sure patient have water in the stomach

Repeat after 20 mins

Dosage:
Children 15 cc (3-5tsp) followed by a glass of water
Adult 30cc (1-2tbsp)followed by a glass of water
STRONG ACID
Coagulative hardening necrosis
Immediate damage to GI tract
1-2 mins complete damage
Burn to mouth, pharynx, esophagus, URT and GIT
Toilet bowl cleaner, HCI, rust remover
ALKALIS
Liquefactive necrosis
Pain-delayed
Longer tissue contact
Mins-hours
Washing soda, ammonia, bleach
MANAGEMENT
Support CAB
IV Fluids replacement ALS
Rapid Transport
GENERAL APPROACH POISONING
C adequate circulation
A adequate airway
B adequate breathing
D Management of drug induced CNS dep.
E electrolyte or metabolic abnormalities
ORGANOPHOSPHATE most commonly associated with
mortality
History taking in poisoning
1. What was ingested
2. Whsn was it ingested
3. How much was ingested
4. What else was taken? Has the pt. taken antidote?
5. Has the pt. vomited, how long after ingestion
6. Has anything has been done before arrival of EMS
Patient assessment: GOAL

Support CAB

Delay absorption
Odor
LOC
VS
Cyanide block aerobic metabolism
Bitter almond
Sodium bicarb- heat acidosis
Hydroxocobalamin
Anticonvulsant
Retiral redness, cherry red
Carbon Monoxide
Colorless, odorless
Gas stoves, room heaters
Cherry red skin- carboxyhemoglobin
Clues no. of pt involved
100% 02 NRM
Hyperbaric 02 tx
Injected poison (Bee,wasp,venom)
cause anaphylaxis
Pt. airway
Remove jewelry
Immobilize limb
Venous constricting band
Downward position
allow slow absorption
Cold pack

SEQUENCE OF ANAPHYLAXIS
Antigen introduced into the body
Antigen antibody reactiob
Release of mast cell chem. Mediator
Chemical medications exert their effect on end organs
A.
B.

Stimulants
Cocaine, amphetamines
Depressant
Normal functions of CNS
Ethyl alcohol
Affects judgement
Can mimic the ff:

Diabetes

Head injury

Epilepsy

Drug reaction
Disulfiran (Antabuse)
30-8 hours
Treatment for alcoholics

ALCOHOL WITHDRAWAL SYNDROME

6-28 hours after alcohol
Consumption is stopped
Tremors, anxiety, sweating
DELIRIUM TREMENS
Shaking frenzy from ethanol withdrawal
24-2 weeks
High BP, RR and Temperature
NARCOTICS
Pain killer
Control diarrhea
Overdose ; pin point pupils
Withdrawal: dilatation, nasal congestion
BARBITURATES
Relieve anxiety
Promote sleep
HALLUCINOGEN
Flushed face; sudden mood change
Angels dust
Pencyclidine reduce pain
DESIGNERS DRUG
Laboratory made
Synthetic
Snorted, smoked, ingested
FENTANYL - China white; Persian white, narcotic
METHYLENEDIOXYMETHAMPETHAMINE
Ecstasy/love drug
Drowsiness 1-3 days
Adverse effect: heart injury, disseminated intravascular
coagulation (DIC)
Cause of death: disturbance in temperature
GAMMA
-

HYDROXYBUTYRATE 6 horus
Narcolepsy
Slow wave sleep
Georgia homeboy
Relaxation

AMPHETAMINE
Crystal meth
Snorted
2-4 days withdrawal
COCAINE
Crack, cola, crack
60% patent smoke

CAB
Snorting can destroy nasal septum

SOLVENT
Glue, paint
1st sniffed
2nd soaking cloth
3rd bagging
Sudden Sniffing Death Syndrome (Cardiac Arrhythmia)
Treatment: Activated charcoal
WATUSI POISONING
Dancing firecracker

Patients skin : BRUSH the powder

Liquid: irrigate the skin for 20 mins (attention to skin
crease and fingernails)
Patients eyes: 20 mins flushing
2-3 inches away
Cover with moist dressing
ACETAMINOPHEN
ARSENIC
ATROPINE
BENZODIAZIPINE
Carbon monoxide
CYANIDE
NITRATES
OPIATES
MERCURY
ORGANOPHOSPHATE
LEAD
METHANOL

Incubation
Acute infection
2-4 weeks
Fever, sore throat, lymphadenopathy
Seroconversion
6-12 weeks
Immune system is still fighting
Should be tested
2-3 weeks after exposure
6 weeks 3 months
6 months

ABSORBED POISON
Plants, pesticides
Liquid/powder
Burns, itching

Across placenta 20th week of gestation

Precaution in dealing HIV positive patient

1. Observe and practice Universal Precaution
2. Restrict pregnant EMT from contact
3. Protect pt from acquiring infection from you or your
crew
4. Assume that every patient you treat is HIV+

HEROINE
From morphine, nalagesia
Naloxone antidote
Chasing the dragon

3.

ANTIDOTE
N-Acetylcystene
BAL
Physostigmine
Flumazeril
oxygen
Sodium Nitrate
Hydorcobalamine
Methylene Blue
Nalaxone
Dimecaprol
Atropine
Edetate Calcium Disodium
Ethanol

1.

When in doubt

Assume that containers were full

Entire contents were ingested

2. Always:

Bring sample of material

Save for analysis if vomits

Call poison center for advice

3. Cause of death in ingested poison

Antidep

Pain relievers

Sedatives

Cardio meds
PATIENT ASSESSMENT INHALED POISON
Precaution

Thorough scene size up HAZMAT

Have sample of substance involved

Fire and explosion precaution

If the scene is not safe do not enter

INFECTIOUS DISEASES
AIDS
Mode of transmission
1. Sexual Contact semen, saliva, blood
2. Parenterally blood products/ infected needles

After infection
8 years/9years/15 years adult
2 years children
Aids Related Complex
Seroconversion stage
Weight loss > 10%
diarrhea for > 1 month
fever
night sweats
True AIDS
life threatening
opportunistic infection:
a. Pnuemocystis carina
Most common
Leads to aids diagnosis
Life threatening
b. Candida Albicans
Thrush in infants
Yeast infection
Normal if milk-fed
c. Cypromegalovirus pregnant)
d. Kaposis Sarcoma
Others:
Fungi, Virus, Parasites, bacteria
AIDS Dementia Complex
Infection of CNS cells
Cerebral atrophy
Cognitive dysfunction
Declining motor performance
Behavioral changes
Safety

Precautions AIDS
BSI
H.W between patients
Clean blood spills with bleach solution
All sharps infectious
Do not recap
Wear mask

Treatment:
1. Support care
2. No immunization
3. Post exposure prophylaxis treatment
- 3 hours of significant exposure
Recommendation
Zidovudine
lamivudine

Indinavir

relfircivir

Diagnosis:
Elisa 2 weeks from exposure to confirm
Western Blood confirmatory after Elisa
KILLING HIV
A. HEAT
56C (10-20mins)
Lyophilized protein prep 68C after 2 hours
B. DISINFECTANT
Glutaraldehyde and hydrochloride low conc.
Isopropyl/Ethanol (40-70%)
Inactivates HIV
Less effective if dried HIV
Detergents and high and low ph solutions
C. DRYING
Reduce viral ineffectivity
Dried HIV in salt solution may still detected after a
week
Dried serum or blood unlikely to be significant
infection risk
EMT Indirect contact
Disinfect - Drying
NATURAL HISTORY

Lymphadenopathy

Flu like symptoms

2 weeks

Fever and Malaise

Asymptomatic infection (1-10 years)
50% develop true aids within 10 years
RNA VIRUS
Retrovirus uses reverse transcriptase enzyme
Target cells is T-helper(CD4 positive cell)
2 virus can combine in one celldiversity
HEPATITIS inflammation of the liver
HEPA A & E oral-fecal route
HEPA BCD - Parenteral
HEPATITIS A

Fecal-oral (improper food handling)

Can survive to 4 hours

Incubation 25-40 days

Does not cause CLD

SIGN AND SYMPTOMS

Dark urine
Possible jaundice
Abd. discomfort

HEPATITIS B

Parenteral

Blood borne, sexual, perinatal

Incubation: 42-160 days

Can survive up to 7 days

Cause CLD and Liver cancer, Chronic infection

Sign and SX: 2-3 months non specific
Joint pain
Dark urine
Clay colored stool
Jaundice
Supportive care
o
BSI and HW
o
Inactivated by 0.1% glutaraldehyde household bleach
o
Inactivated by heating 98C for 2 mins
o
Resistant to detergent and alcohol
o
With vaccine
HEPATITIS C Non A, non B
Parenteral

Bloodborne, sexual, perinatal

Liver Transplant possible
Chronic Carrier
Chronic Liver Disease and infection
Sign and Symptoms
Joint pain
Dark urine
Less progression to jaundice
Treatment support care

BSI and HW

No recognized from prophylactic IgG

HEPATITIS D

Delta virus

Requires HBV

Parenteral, blood and body fluids

Chronic infection

CLD possible

Coinfection can be prevented by vaccine

Non for superinfection

Vaccine HBV indirectly prevents HDV

HEPATITIS E (Non A Non B)

Oral fecal transmission

Enterically transmitted

Sources: feces

Incubation: 15-60 days

Patients are usually travellers

HBV not effective HEV

General Safety: Hepatitis

BSI, safety

Observe and practice universal precaution

Gloves

Needle precaution

Bag label blood sampler / contaminated linens

Obtain immunization

Wash blood spills with bleach solution

Assess personal behavior risks

Stay in touch in the hospital to w/c patient was

transported for Frup dx
TUBERCULOSIS

Mycobacterium tuberculosis

Transmission: droplet ; airborne

Direct infection trough non-contact skin extra

pulmonary TB

Obligate aerobe

Grows outside the cell

Gram + Bacillus

Grow very slowly (chronic illness)

Characteristic:

Resistant to drying, acid, alkali

Sensitive to UV, phenol, Nahypochloride, heat

Remains viable in dark areas for months

Untreated TB develop in 1-2 years

Incubation: 4-12 weeks

Clinical manifestation 6-12 months after infection

X-Ray confirmatory

acid fast staining

cell mediated immune response walls of bacteria

(tubercle)

untreated hematemesis

severe form hemothorax

ALS must have exhaust ventilation

TX and PV:

BSI
Wear mask
Routine TB testing of EMS personnel
Expose repetition of skin test
INH prophylaxis, routinely in <35years of ages
+PITS

1.
2.
3.
4.

MEDICATION: (longterm)
Isoniazid, ritampicin, Ethambutol, Strep, Pyra
SYPHILIS

Spirocheles

Treponcemapallidum

Transmission sexual contact, mother to fetus, direct

contact &exudales

Needle stick uncommon

PRIMARY

Chancre painless ulcer, site of entry

Regional Lymphadenopathy
SECONDARY

Bacteremia 6 weeks after chancre healed

6-12 weeks (fever, rashes)

Peak 3-4 hours

Lesion may reappear up to 1 year

Fishy odor female

LATENT

1-3 years/rest of patients life

Early < 2 years
Late phase > 2 years
Untreated patient develop tertiary syphilis 3-25 years

TERTIARY not contagios

a. Gumma lesion of skin, bone
Painless & sharp borders
Bone & deep gnawing pain
b. Cardiovascular syphilis
10 years after infection
Aneurysm
c. Neurosyphilis
Meningitis
Loss of reflexes
TX & PV

*Full Isolation when transporting

BSI
Avoid contact & respi secretions
Mask pt& yourself
If Close contact / exposure occurs

HW frequently

Air out Vehicle

Send linens to laundry

Immunization (no routine vacc for EMS personnel)

RABIES

Lyssavirus

Viral encephalitis

Transmission
o
-saliva containing virus after a bite
scratch of infected animals

Negribodies activation and release in their brains after

bitting

Death usually 2-6 days & intervention

Death respiratory failure

S/SX:

3 PHASES of Rabies
A.

B.

C.

Syphilis
Avoid contact & skin lesions
BSI
HVV
Contagious patient are in primary, secondary and early
latent stage

MENINGITIS

Meningococcal Meningitis

Neisseria Meningitis children

Bacteria, virus, fungi

FUNGUS Cryprococcus Neoformans
VIRUS Enterovirus
STREPTOCOCCUS P. children
Transmission: Airborne

Colonizes the throat respi sections

Direct contact & respi secretion

Infant (carriers) 6 months- 2 years

S/SX
PV & TX:

Seizure, high fever, rapid onset, nuchal rigidity,

progressing ecchymosis, delirium

Apprehension
Headache
Spasm on swallowing muscle result in hydrophobia and
salivation

TX & PV
1.
2.
3.
4.
5.
6.

Prodromal Phase

2-3 days

Fever, headache

Copious salivation (laryngospasm)

Trismus (sadness)

ANV is affected
Anger Stage

Restless

Disoriented

2-4 days

Seizure

Application of mechanical restrain

Neurologic Stage

Paralytic Stage

Paralysis of throuat and face

Begin & the body part that was bitten

Terrified of H@)

Anxious, hyperactive

2-4 days
BSI, safety
Free bleeding and drainage
Vigorously clean wound with soap and water
Tetatus Prophylaxis
Human Rabies IgG
Human Diploid cell rabies vacc or Rabies vacc for
higher risk person animal care workers, animal shelter
personnel

Intellectual Property of Mr. PJBautista =)