It is considered the state in which the rate, depth, timing, and

rhythm, or the pattern of breathing is altered.

When the breathing pattern is ineffective, the body is most

likely not getting enough oxygen to the cells.

Respiratory failure may be correlated with variations in

respiratory rate, abdominal, and thoracic pattern.
RELATED FACTORS

heart failure, hypoxia, airway obstruction, diaphragmatic

paralysis, infection, neuromuscular impairment, trauma or
surgery resulting in musculoskeletal impairment and/or pain,
cognitive impairment and anxiety, diabetic ketoacidosis,
uremia, thyroid dysfunction, peritonitis, drug overdose,
AIDS, acute alcohol withdrawal, cardiac surgery,
cholecystectomy, liver cirrhosis, craniocerebral trauma, disc
surgery, lymphomas, renal dialysis, seizure disorders,
spinal cord injuries, mechanical ventilatory assistance and
pleural inflammation.
HOW ALTERATION MAY HAPPEN (in an instance)

Normal physiology 1:The lungs are like sponges; they

cannot expand on their own. Muscles in your chest and
abdomen contract (tighten) to create a slight vacuum
around your lungs. This causes air to flow in. When you
exhale, the muscles relax and the lungs deflate on their
own, much like an elastic balloon will deflate if left open to
the air.
Alteration 1: Stab wound penetrating the chest- allows
environmental air to get inside - air collects in between the
parietal and visceral pleurae - alters the balance between
the lungs and the pleurae -lung collapse.
HOW ALTERATION MAY HAPPEN (in an instance)

Normal physiology 1:The lungs are like sponges; they

cannot expand on their own. Muscles in your chest and
abdomen contract (tighten) to create a slight vacuum
around your lungs. This causes air to flow in. When you
exhale, the muscles relax and the lungs deflate on their
own, much like an elastic balloon will deflate if left open to
the air.
Alteration 2: Respiratory muscle weakness - ineffective
contraction to tighten the chest- no sufficient vaccum to
allow air to flow in
CHOKING

blockage of the upper airway by food or other objects -

no gas exchange

mechanism of gas exchange- inhale (breathe in), air enters

lungs - oxygen from the air moves from the lungs to the
blood for circulation ( at the same time, carbon dioxide
moves from the blood to the lungs and is exhaled (breathe
out)
HOW ALTERATION MAY HAPPEN (in an instance)

Normal physiology: inhale (breathe in), air enters lungs -

oxygen from the air moves from the lungs to the blood for
circulation ( at the same time, carbon dioxide moves from
the blood to the lungs and is exhaled (breathe out)
Alteration 1: no air flow---stop breathing
Alteration 2: no gas exchange at the cellular level---
insufficient carbon dioxide (CO2) excretion---alveolar
hypoventilation- arterial hypercapnia (elevation in the partial
pressure of carbon dioxide (PaCO2) above 45 mm Hg)
 Heart Attack
myocardial infarction- caused by coronary artery disease --
Normal mechanism: coronary arteries supply blood to the
myocardial cells for its normal electrical and muscular
function
Pathologic: buildup of plaque in the arteries --narrowed or
blocked arteries- low or no oxygen supply to the heart
Alteration: no cellular gas exchange-- within 10 seconds-
cells are ischemic-- decreased electrical and muscular
function-- anaerobic metabolism
 STROKE
blood supply to part of the brain is interrupted or reduced
brain tissue not supplied with oxygen and nutrients
brain cells begin to die
Ischemic- artery that supplies oxygen-rich blood to the brain
becomes blocked.Blood clots often cause the blockages
Hemorrhagic-an artery in the brain leaks blood or ruptures
(breaks open). The leaked blood puts too much pressure on
brain cells, which damages them.
Transient ischemic attack- blood flow to the brain is blocked
for only a short time—usually no more than 5 minutes
 Heavy Bleeding
Blood pressure falls because the amount of fluid left in the
blood vessels is insufficient.
The body's oxygen supply is drastically reduced because
the number of oxygen-carrying red blood cells decreases so
quickly.
 Heavy Bleeding
Arterial bleeding occurs in the arteries, which transport
blood from the heart to the body.
Venous bleeding happens in the veins, which carry blood
back to the heart.
Capillary bleeding takes place in the capillaries, which are
tiny blood vessels that connect the arteries to the veins.

arterial bleeding comes out in spurts, venous bleeding flows

steadily, and capillary bleeding trickles from the body
POISONING
Poison is anything that kills or injures through its chemical actions

Reduction in free toxin level can be achieved by specific and non-specific agents that bind
to the toxin.

Poison – any substance that through its chemical action

and sometimes, physical action, impairs, injures or kills
an organism. It includes cases of overdosage.
 Routes:
1. Ingestion
2. Inhalation
3. Absorption ( mucosa, ocular, dermal)
4. Injection
Related to external or internal blood/fluid loss
(most common cause of shock); hemorrhage,
burns, dehydration

Related to ischemia/impairment in tissue

perfusion from myocardial infarction, serious
arrhythmia, or congestive heart failure. All of
these result in decreased cardiac output.
 Types of Results from inadequate vascular tone.
Distributive
SHOCK
Blood volume remains normal
Vascular space increases dramatically
because of massive vasodilation

1.Neurogenic Blocking of the sympathetic NS in SCI at

or above T5 leads to massive peripheral
va s o d i l at i o n f ro m a n u n o p p o s e d
parasympathetic NS.
> Hypotension and bradycardia
2. VASOGENIC Related to allergens (anaphylaxis), or
ANAPHYLACTIC
peripheral neuropathies, all resulting in
venous pooling and decreased blood
return to the heart, which decreases
cardiac output over time. Warm skin,
bronchoconstriction rashes may be
observed with products of inflammation
3.Septic Related to endotoxins released from
bacteria, which causes vascular pooling,
diminished venous return and reduced
cardiac output. S/S with fever
 STAGES OF HYPOVOLEMIC SHOCK
STAGE SIGNS AND SYMPTOMS CLINICAL DESCRIPTION

STAGE I: Apprehension and Arteriolar constriction

INITIAL restlessness (first Increased production of
STAGE signs of shock) ADH
Blood loss of Increased heart rate Arterial pressure is
less than 10%. Cool, pale skin maintained
Compensatory Fatigue Cardiac output usually
mechanisms normal (for healthy
triggered. individuals)
Selective reduction of
blood flow to skin and
muscle beds
STAGE II: First clinical sign: Marked reduction in cardiac
COMPENSATORY hypotension due to output
STAGE decreased CO Arterial pressure decline
Flattened neck veins (despite compensatory
Bloodvolume and delayed venous arteriolar vasoconstriction)
reduced by 15 filling time Massive adrenergic
to 25%. Increased pulse and compensatory response
Decompensation respirations resulting in: tachycardia,
begins. Pallor, diaphoresis and tachypnea,cutaneous
cool skin vasoconstriction, and oliguria
Decreased urinary Decreased cerebral perfusion
output Activates renin-angiotensin
Sunken soft eyeballs and aldosterone mechanism
Confusion
STAGE Edema Rapid circulatory
III: Increased blood deterioration
PROGRESSIVE viscosity Decreased cardiac
STAGE; loss of
25-40% Excessively low output
blood pressure Decreased tissue
Dysrhythmia, perfusion
ischemia and MI Reduced blood
Weak, thready, or volume
absent peripheral
pulses
STAGE IV: Profound hypotension, Cell destruction so severe
Irreversible
STAGE; blood loss
unresponsive to death is inevitable
of more than 45% vasopressor drugs Multiple organ system
Severe hypoxemia, failure
unresponsive to oxygen  It is the nurse’s responsibility
administration to recognize the signs and
Anuria, renal shutdown, symptoms of shock. Every effort
metabolic acidosis should be made to prevent the
Heart rate slows, BP devastating clinical course that
falls, with consequent the progression of shock can
cardiac and respiratory take.
arrest
PHARMACODYNAMICS OF
COMMON EMERGENCY MEDICATIONS
APPLIED TO PATHOPHYSIOLOGIC
CHANGES IN MEDICAL EMERGENCIES
EPINEPHRINE

Drug Classification: Adrenergic Agonist

Indications: management of reversible airway disease due to asthma
or COPD, severe allergic reactions, part of advanced cardiac life
support, cardiac arrest, anesthesia
Mechanism of Action: results in the accumulation of cyclic adenosine
monophosphate at beta-adrenergic receptors; produces
bronchodilation; results in vasoconstriction; inhibits the release of
mediators or immediate hypersensitivity reactions from mast cells
Adverse Effects/ Side Effects: nervousness, restlessness, tremors,
headache, insomnia, angina, arrhythmias, hypertension, tachycardia,
n/v, bronchospasm
EPINEPHRINE (CONT.)

Dosage:
SC, IM - 0.1-0.5 mg (dose not to exceed 1 mg) may repeat q 10-15
min
for anaphylactic shock
IV - 0.1-0.25 mg q 5-15 min;may be followed by 1-4 mcg/min
continuous infusion
Nursing Considerations:
1. 1. Epinephrine should be administered at the onset of bronchospasm

2. 2. Tolerance may develop with prolonged/excessive use

3. 3. Do not administer if the solution is pinkish or brownish or contains

4. a precipitate
5. 4. For anaphylactic shock, volume replacement should be

a. administered concurrently with epinephrine

EPINEPHRINE (CONT.)

1. 5. Instruct patient to contact health care provider immediately if

2. shortness of breath is not relieved by medication or is
3. accompanied by chest pain, dizziness, or diaphoresis
6. For IV route, dilute 1 mg (1ml) of 1;1000 solution in at least 10 ml
of 0.9% NaCl for injection to prepare a 1:10,000 solution; discard if
not used within 24 hours
7. Administer each 1 mg of 10 ml of 1:10,000 solutions over at least 1
min, more rapid administration may be used during cardiac
resuscitation; follow each dose with 20 ml IV flush
 An agonist is a drug that binds to
EPINEPHRINE the receptor, producing a similar
ANAPHYLAXIS Epinephrine
response to the intended
ACTION: injection is used chemical and receptor. ...
Sympathomimetic to treat severe Whereas an antagonist is a drug
that binds to the receptor either
allergic reactions on the primary site, or on another
producing
physiological effects
(anaphylaxis) site, which all together stops the
receptor from producing a
characteristic of the
response
sympathetic nervous
system by promoting vasoconstrictor effects
the stimulation of
sympathetic nerves prevents or decreases Activation of
upper airway mucosal edema the beta2
SNS connects the internal organs to (laryngeal edema), receptor leads
the brain by spinal nerves. When hypotension, and shock to vascular and
stimulated, these nerves prepare the nonvascular
organism for stress by increasing the Beta 2 agonist: relaxation of smooth muscle
heart rate, increasing blood flow to the bronchial muscles relaxation
muscles, and decreasing blood flow to
the skin. bronchodilator effects
ANAPHYLAXIS
� a severe allergic reaction of rapid onset
affecting many body systems. It is due to the
release of inflammatory mediators and
cytokines from mast cells and basophils
� closely linked to IgE activation of mast cells
with subsequent release of preformed
mediators, including histamine, neutral
proteases (tryptase and chymase), and
proteoglycans (eg, heparin) from intracellular
granules
� release of chemicals leads to shock —

blood pressure drops suddenly and airways

narrow-----blocking breathing
EPINEPHRINE
Positive inotropes
CARDIAC ARREST strengthen the force
of the heartbeat.
ACTION: Alpha Chronotropic drugs may
Negative inotropes
Adrenergic: constriction change the heart rate and
weaken the force of
of BV rhythm by affecting the
the heartbeat.
electrical conduction system
Beta 1 agonist:
of the heart and the nerves
(+) inotropic,
that influence it, such as by
(+)chronotropic changing the rhythm Sympathomimetic: SNS
produced by the sinoatrial connects the internal
increase node. Positive chronotropes organs to the brain by
myocardial and increase heart rate; negative spinal nerves. When
cerebral blood flow chronotropes decrease heart
stimulated, these nerves
during CPR rate.
prepare the organism for
stress by increasing the
increased heart heart rate, increasing
rate, myocardial Renin splits blood flow to the muscles,
contractility, and angiotensinogen, a large and decreasing blood flow
renin release via protein that circulates in the to the skin.
beta-1 receptor bloodstream, into pieces.
THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
Angiotensin I, which is relatively inactive, is split into pieces by
angiotensin-converting enzyme (ACE). One piece is angiotensin II, a
hormone, which is very active.

Angiotensin II causes the muscular walls of small arteries

(arterioles) to constrict, increasing blood pressure. Angiotensin II
also triggers the release of the hormone aldosterone from the adrenal
glands and vasopressin (antidiuretic hormone) from the pituitary
gland.

Aldosterone and vasopressin cause the kidneys to

retain sodium . Aldosterone also causes the kidneys
to excrete potassium. The increased sodium causes
water to be retained, thus increasing blood volume
and blood pressure.
AMIODARONE

� Amiodarone is primarily indicated to treat ventricular fibrillation

(VF) and ventricular tachycardia (VT) that occurs during cardiac
arrest
� restore normal heart rhythm and maintain a regular, steady
heartbeat
� an anti-arrhythmic drug (blocks certain electrical signals in the
heart that can cause an irregular heartbeat)
� multiple effects on myocardial depolarization and repolarization
� primary effect is to block the potassium channels, but it can also
block sodium and calcium channels and the beta and alpha
adrenergic receptors.
AMIODARONE

Drug Classification: Antiarrhythmics

Indications: management and prophylaxis of life threatening
ventricular arrhythmias; part of of Advanced Cardiac Life Support;

Mechanism of Action: prolongs potential and refractory period;

inhibits adrenergic stimulation; slows sinus rate, increases PR and
QT interval; and decreases peripheral vascular resistance

Adverse Effects/ Side Effects: dizzines, fatigue, malaise, headache,

dry eyes, optic neuritis, photophobia, ARDS, bradycardia,
hypotension, anorexia, constipation, n/v, abdominal pain,
AMIODARONE (CONT.)

Dosage:
IV - 150 mg over 10 mins, followed by 360 mg over the next 6 hrs
and then 540 mg over the next 18 hrs. Continue infusion until oral
therapy is started

Nursing Considerations:
1. 1. ECG should be monitored continuously during IV therapy; monitor
a. HR and rhythm
2. 2. Assess patient for signs of pulmonary toxicity (rales/crackles,
a. decrease breath sounds, fatigue, dyspnea, cough, fever)
3. 3. Instruct patient to take medication exactly as prescribed
4. 4. Teach patients to monitor pulse daily and report abnormalities
5.
POTASSIUM-CHANNEL BLOCKERS (CLASS III
ANTIARRHYTHMICS)
� These drugs bind to and block the potassium channels that are
responsible for phase 3 repolarization. Therefore, blocking these
channels slows (delays) repolarization, which leads to an increase in
action potential duration and an increase in the effective refractory
period (ERP).

� On the electrocardiogram, this increases the Q-T interval

� By increasing the ERP, these drugs are very useful in suppressing

tachyarrhythmias
� Advanced cardiac life support (ACLS) guidelines recommend using
amiodarone only after epinephrine and vasopressin have failed to
convert VF/VT (E_V_A)
ATROPINE
Atropine is used to help keep
heart rates stable after a heart
attack.
mainly in the management of
bradycardia
increases the heart rate and
improves the atrioventricular
conduction by blocking the
parasympathetic influences on
the heart.
� reduce salivation and bronchial
secretions before surgery or as
an antidote for overdose of
cholinergic drugs or mushroom
poisoning
Anti-cholinergic
Cholinergic Symptoms are
predominantly caused by
activation of muscarinic receptors
that control the parasympathetic
nervous system. bradycardia,
wheezing, diaphoresis, miosis,
diarrhea, and salivation.
ATROPINE
Drug Classification: Antiarrhythmics
Indications: given preop to decrease oral and respiratory secretions;
treatment of sinus bradycardia and heart block; reversal of adverse
muscarinic effects of anticholinesterase agents; treatment of
anticholinesterase poisoning

Mechanism of Action: Inhibits the action of acetylcholine at

postganglionic, thus, reducing secretions in the mouth and
respiratory passages; relieves the constriction and spasm of the
respiratory passages
Adverse Effects/ Side Effects: drowsiness, confusion, blurred vision,
dry eyes, tachycardia, palpitations, dry mouth, constipation, urinary
retention, decreased sweating
ATROPINE (CONT.)

Dosage:
IV - For bradycardia, 0.5-1.0 mg; may repeat as needed q 5 mins
(q 3-5 mins in Advanced Cardiac Life Support)

Nursing Considerations:
1. 1. Assess VS and ECG tracing during therapy

2. 2. MIO because atropine may cause urinary retention

3. 3. Assess patients for abdominal distention and auscultate for bowel

a. sounds
4. 4. Drug may cause drowsiness
CALCIUM GLUCONATE
� Calcium is important for the
strength of contraction of
cardiac tissue. It is used to
stabilize myocardium and help
get a patient out of a lethal
rhythm.
� used to manage hypocalcemia,
cardiac arrest, and
cardiotoxicity due to
hyperkalemia or
hypermagnesemia (high
potassium and magnesium
levels in the blood)
� .
� Calcium can also be used to
protect against a number of
metabolic conditions that
cause pulseless electrical
activity, including raised blood
potassium levels, lowered
blood calcium levels and
overdose of magnesium or
calcium channel blocking
drugs.
CALCIUM GLUCONATE
Drug Classification: Mineral and electrolyte supplements
Indications: treatment and prevention of hypocalcemia; emergency
treatment of hyperkalemia and hypermagnesemia and adjunct in
cardiac arrest

Mechanism of Action: acts as an activator in the transmission of nerve

impulses and contraction of cardiac, skeletal and smooth muscle

Adverse Effects/ Side Effects: syncope, tingling, arrhythmias,

bradycardia, n/v, hypercalciuria, phlebitis
CALCIUM GLUCONATE (CONT.)
Dosage:
IV – for emergency treatment of hypocalcemia and cardiac
standstill; 7-14 mEq/L

Nursing Considerations:
1. 1. Observe patient for symptoms of hypocalcemia (paresthesia, muscle

1. twitching, laryngospasm, arrhythmias, Chvostek’s or Trousseau’s sign)

2. 2. Protect patient by raising siderails and keeping bed in low position
3. 3. Monitor BP, pulse, and ECG
4. 4. Assess for IV patency; give solution through a small-bore needle
5. 5. Administer medication slowly
6. 6. Patient should remain in recumbent position for 30-60 mins after
1. administration
SODIUM BICARBONATE

� Sodium bicarbonate is used

when the code response team
believes that the patient may
be acidotic because the drug
helps to increase serum PH,
which in turn could prevent
further coding.
SODIUM BICARBONATE
Drug Classification: Alkalinizing agent
Indications: management of metabolic acidosis; alkalinizes urine and
promote excretion of drugs in overdosing

Mechanism of Action: releases bicarbonate ions, which is capable of

neutralizing gastric acid

Adverse Effects/ Side Effects: edema, flatulence, metabolic alkalosis,

hypernatremia, hypocalcemia, hypokalemia, sodium and water
retention, tetany
SODIUM BICARBONATE (CONT.)
Dosage:
IV – for cardiac arrest, 1 mEq/kg, may repeat 0.5 mEq/kg q 10 mins

Nursing Considerations:
1. 1. MIO, weigh patient daily, and assess lung sounds

2. 2. Observe IV site closely

3. 3. Administer IV push in arrest situations

4. 4. Use prefilled syringes to ensure accurate dosage; dose should be

1. based on ABG results

VASOPRESSIN
Vasopressin is a primary drug
used in the pulseless arrest
algorithm
antidiuretic action on the
collecting ducts of the kidney
Vasopressin is a potent
vasopressor for improving organ
perfusion during septic shock.
use of vasopressin in the ICU
vasopressin deficiency in
vasodilatory shock and
advanced shock from any cause
exogenously administered
vasopressin can restore
vascular tone.
relative deficiency of plasma
levels and hypersensitivity to its
vasopressor effects during septic
shock
VASOPRESSIN
Drug Classification: Antidiuretic hormone

Indications: diabetes insipidus due to deficient antidiuretic hormone;

management of pulseless VF/ VT unresponsive to initial shocks

Mechanism of Action: alters the permeability of the renal collecting

ducts, allowing reabsorption of water; acts as a nonadrenergic
peripheral vasoconstrictor

Adverse Effects/ Side Effects: dizziness, angina, chest pain,

abdominal cramps, belching, diarrhea, flatulence, n/v, sweating,
trembling, fever, water intoxication
VASOPRESSION (CONT.)
Dosage:
IV – pulseless VF/VT, 40 units as a single dose

Nursing Considerations:
1. 1. Monitor ECG

2. 2. Monitor urine osmolality and urine volume frequently to determine

1. effects of dehydration; assess for dehydration

3. Administer as a single IV push dose during cardiac arrest
4. Monitor serum electrolytes
5. Monitor for s/s of water intoxication (confusion, drowsiness, headache, weight
gain, difficulty urinating, seizures, and coma)
DOPAMINE
used to treat insufficient
cardiac output and for
hypotension.
Dobutamine ---acute but
Dopamine and dobutamine are
potentially reversible heart
the drugs of choice to improve
failure, such as which occurs
cardiac contractility, with
during cardiac surgery or in
dopamine the preferred agent in
cases of septic or cardiogenic
patients with hypotension.
shock-----(+) inotropic
Vasodilators relax vascular
smooth muscle and reduce the
sytemic vascular resistance in CHF to increase cardiac
(SVR)------improved forward output
flow-----improved cardiac output
DOPAMINE
Drug Classification: Inotropic vasopressor

Indications: adjunct to standard measures to improve: blood measure,

cardiac output, urine output in treatment of shock unresponsive to
fluid replacement

Mechanism of Action: stimulate dopaminergic receptors, producing

renal vasodilation; stimulates beta adrenergic receptors producing
cardiac stimulation and renal vasodilation

Adverse Effects/ Side Effects: headache, mydriasis, dyspnea,

arrhythmias, hypotension, angina, palpitations, vasoconstriction,
n/v
DOPAMINE (CONT.)
Dosage:
IV – 2-10 mcg/kg/min; infusion rate may be increased as needed

Nursing Considerations:
1. 1. Monitor BP, HR, ECG, capillary refill; report changes in V/S or

1. arrhythmias
2. 2. MIO frequently; report decrease in urine output promptly
3. 3. Assess peripheral pulses and extremities
4. 4. Assess IV site for extravasation
5. 5. Infusion must be administered via infusion pump to ensure precise
1. amount delivered
NITROGLYCERIN
Drug Classification: Antianginal, Nitrates

Indications: angina pectoris, adjunct treatment for MI, CHF

Mechanism of Action: increase coronary blood flow by dilating

coronary arteries and improving collateral flow to ischemic
regions; produces vasodilation; reduces myocardial oxygen
consumption

Adverse Effects/ Side Effects: dizziness, headache, restlessness,

weakness, blurred vison, hypotension, tachycardia, syncope,
abdominal pain, n/v
NITROGLYCERIN (CONT.)
Dosage:
SL – 0.3-0.6 mg; may repeat q 5 mins for 15 mins for an acute
attack
Transdermal patch – 0.1-0.6 mg/hr; patch should be worn 12-14
hr/day

Nursing Considerations:
1. 1. assess location, duration, intensity, and precipitating factors of pain

2. 2. Monitor BP and pulse before and after administration

3. 3. For SL, tablet should be held under tongue until dissolved

4. 4. For transdermal, apply to hairless site

5. 5. caution patient to change positions slowly

6. 6. At first sign of attack, advise patient to sit down and use medication
DIPHENHYDRAMINE
Drug Classification: Antihistamine

Indications: relief of allergic symptoms caused by histamine release

including Anaphylaxis, allergic rhinitis, and allergic dermatitis

Mechanism of Action: antagonizes the effects of histamine at H1

receptor sites, does not bind to or inactivate histamine

Adverse Effects/ Side Effects: drowsiness, dizziness, headache,

blurred vision, tinnitus, hypotension, palpitation, anorexia, dry
mouth, constipation, diarrhea, urinary retention, photosensitivity
DIPHENHYDRAMINE (CONT.)
Dosage:
IM, IV – 10-50 mg q 2-3 hrs as needed (may need up to 100 mg dose,
not to exceed 400 mg/day)
Nursing Considerations:
1. 1. for treatment of anaphylaxis, assess for urticarial and for patency of

1. airway
2. 2. Administer IM into well-developed muscle, avoid SC
3. 3. IV, may be given diluted in 0.9% NaCl
4. 4. Inject 25 mg over at least 1 min, for IV route
5. 5. may cause drowsiness, and advise patient to wear sunscreen and
1. protective clothing
NALOXONE
� naloxone or other opioid
antidotes to an overdose—
either accidental or stemming
from drug abuse
sedation, dizziness, nausea,
vomiting, constipation, physical
dependence, tolerance, and
respiratory depression
opioid receptor antagonist
binds to opioid receptors and
reverses or blocks the effects of
other opioids---- reverses the
effects of opioid drugs, restoring
normal respiration
MORPHINE
Drug Classification: Opioid Analgesic

Indications: severe pain, pain associated with MI

Mechanism of Action: binds to opiate receptors in the CNS; alters

the perception and response to painful stimulus while producing
generalized CNS depression

Adverse Effects/ Side Effects: confusion, sedation, dizziness,

headache, hallucinations, blurred vision, hypotension,
bradycardia, constipation, n/v, urinary retention, flushing,
sweating, dependence
MORPHINE (CONT.)
Dosage:
IM, IV, SC – for moderate to severe pain, 4-10 mg q 3-4 hr

Nursing Considerations:
1. 1. assess type, location, and intensity of pain

2. 2. prolonged use may lead to physical and psychological dependence

1. and tolerance
3. 3. discontinued gradually to prevent withdrawal symptoms
4. 4. use IM or IV route, because morphine is irritating to SC tissues
5. 5. solution is colorless, do not administer discolored solution
6. 6. dilute solution with 5 ml of sterile water or 0.9% NaCl for injection
7. 7. administer via infusion pump 2.5-15 mg over 4-5 min
LORAZEPAM
Drug Classification: Benzodiazepine

Indications: management of status epilepticus

Mechanism of Action: depresses the CNS, by potentiating GABA, an

inhibitory neurotransmitter

Adverse Effects/ Side Effects: dizziness, drowsiness, headache,

blurred vision, respiratory depression, bradycardia,
hypotension, constipation, diarrhea, n/v, rashes
LORAZEPAM (CONT.)
Dosage:
IM – 0.05 mg/kg
IV – 0.05 mg/kg up to 4 mg

Nursing Considerations:
1. 1. assess location, duration, characteristics, and frequency of seizures

2. 2. dilute immediately before use with sterile water or 0.9% NaCl

3. 3. administer IV, at a rate of 2 mg over 1 min

NALOXONE
Drug Classification: Opioid Antagonists

Indications: reversal of CNS depression and respiratory depression

because of opioid overdose; management of circulatory shock

Mechanism of Action: blocks the effects of opioids (CNS & resp

depression) without producing any opioid-like effects

Adverse Effects/ Side Effects: hypertension, VF, VT, n/v

NALOXONE (CONT.)
Dosage:
IV – overdose of opioids, 0.4 mg; may repeat q 2-3 mins

Nursing Considerations:
1. 1. Monitor RR, rhythm, and depth; ECG, BP, and LOC

2. 2. patients who have been receiving opioids for more than a week are

1. sensitive to the effects of naloxone; dilute and administer carefully

3. 3. Assess patient for level of pain after administration
4. 4. Assess for s/s of opioid withdrawal (vomiting, restlessness,
1. abdominal cramps, increased BP)
5. 5. While giving naloxone, prepare resuscitation equipment, oxygen,
1. vasopressors, and mech vent
6. Titrate dose according to patient’s response
POISONING: SPECIFIC TREATMENTS:
Poisons/Over- Antidotes Rationale
dosage
Paracetamol N-acetylcysteine it restores the liver’s store of
glutathione
Cholinesterase Atropine; Pralidoxine Organophosphates and Carbamates-
Inhibitors inhibit cholinesterase which
hydrolyzes acetylcholine. Increase
acetycholine produces muscarinic
(SLUDGE); nicotinic, and CNS
features.
• Atropine (CNS and muscarinic
effects),
• Pralidoxine ( nicotinic effects esp in
organophosphates
 Poisons/Over-dosage Antidotes Rationale

Lead, mercury, arsenic BAL given IM ( British Anti- Chelating agent

Lewsite or Dimercaprol);
CaEdta ( Calcium Diamidine
ethylenediamine tetracetate)
by IV or IV Infusion

Iron Deferoxamine Chelating agent

Ethanol/ ethyl alcohol Alcohol dehydrogenase has

Methanol, Given IV to maintain blood affinity to ethyl alcohol.
Ethyleneglycol: level of 100-200 mg./dl
Methanol=formal-dehyde
and formic acid;
Ethylene Glycol=
glycoaldehyde
Poisons/Over-dosage Antidotes Rationale

Benzodiazepines Flumazenil Antagonist, reverse the

sedative effect
Beta-Blockers Glucagon Stimulate the beta-
adrenergic nerves.
Carbon monoxide Hyperbarric Oxygen Counteract O2 loss since hgb
hs 200-250 times affinity to
CO2
Methaemoglo- Methylene Blue Reduces methaemoglobin to
binaemia hemoglobin state.
producing – agents

Opiates Naloxone Narcotic Antagonist

Lead, Copper Penicillamine Chelating agent

A chemical compound that binds tightly to metal ions. In medicine, chelating agents are
used to remove toxic metals from the body.
 Poisons/Over- Antidotes Rationale
dosage

Snake Venom Snake antivenin Immunotherapy-specific antibody

Warfarin Vitamin K Promotes hepatic formation of

active prothrombin

Heparin Protamine Sulfate Heparin antagonist

 ASSESSMENT
Clients with
Life Threatening Conditions
/ Medical Emergencies
 Assessment of Clients with Life Threatening Conditions/ Medical Emergencies
Pain assessment

Acute Pain (Specify Type and Location):

Verbal or coded report of the presence of
indicators of severe discomfort (pain) with a
duration of less than 6 months (specify type
and location: joint pain, low back, cervical,
knee pain).
Chronic Pain (Specify Type and Location):
Severe discomfort (pain) with a duration of
more than 6 months (specify type and
location: joint pain, low back, cervical, knee
pain).

Perception of severe discomfort, or pain,

signals possible tissue damage.
Assessment of Clients with Life Threatening Conditions/ Medical Emergencies
Glasgow coma scale

Decerebrate posturing can be

seen in patients with large
bilateral forebrain lesions with
progression caudally into the
diencephalon and midbrain. It
can also be caused by a
posterior fossa lesion
compressing the midbrain or
rostral pons. Though
decerebrate posturing implies a
destructive structural lesion, it
can also be caused by
reversible metabolic
disturbances such as
hypoglycemia and hepatic
encephalopathy.
Assessment of Clients with Life Threatening Conditions/ Medical Emergencies
FOUR Score

-tests crucial brainstem reflexes and

provides information about the
severity of brainstem injury which are
unavailable with the GCS

-recognizes a locked-in syndrome and

a possible vegetative state

-includes signs suggesting brain

herniation
Assessment of Clients with Life Threatening Conditions/ Medical Emergencies
Pressure ulcer assessment tool

The three most widely used

scales are the Braden Scale,
the Norton Scale, and the
Waterlow Scale.
Assessment of Clients with Life
Threatening Conditions/ Medical
Emergencies
TRIAGE

Unstable patients do not have the

energy to tolerate a full history and
examination until after discharge
from the unit.

Common collaborative problems:

Decreased Cardiac Output
Impaired Gas Exchange
Ineffective Tissue Perfusion
Deficient or Excess Fluid Volume
Imbalanced Fluid Volume
Risk for Unstable Blood Glucose
Assessment of Clients with Life Threatening Conditions/ Medical Emergencies
ABCDE basics

https://www.youtube.com/watch?v=9Y4s45Xh6cQ
 Assessment in ED
Circulation Yes Check airway
No Start CPR
Airway Patency Yes Check breathing
No Open airway
Breathing Yes Check effectiveness
No Ventilate patient
Assess for effectiveness Yes Assess Neurologic status
No Determine cause and intervene

Neurologic assessment
Take History
General head to toe Assessment
Primary Assessment
1-2 minutes
Assessment and management

Airway
Breathing
Circulation
Disability
Expose and evaluate
• Airway
1. Assess the airway and determine its
adequacy

2. Create or maintain an airway

3. Recognize the potential for cervical spine

injury and maintain the spine in a safe neutral
position

11
• Breathing
1. Administer high flow oxygen

2. Assess the chest by:

a. Inspection
b. Palpation of the trachea
c. Percussion
d. Auscultation

12
• Circulation
Looking for external hemorrhage

Observing skin color, temperature and CRT

Feeling the pulse

Taking the blood pressure

Neck vessels

14
5Ps in Primary Assessment:
rofuse bleeding
aleness
ulse
ressure (blood)
alpable neck vessels?
• Disability
• 1. GCS
a. Are the eyes open? (4)
b. Talk to the patient (5)
c. Use painful stimulus to finger or toe if
required (6)
2. Assess the pupillary size and response
•
3. Examine for lateralizing signs
– (e.g. differing motor scores on each side and signs
of cord injury
16
• Exposure/Environmental control

1. Expose the patient so that an adequate

complete examination can be performed.

2. Prevent the patient becoming hypothermic,

measure their temperature

17
Adjuncts to Primary Survey
• Chest and pelvic x-rays
• Diagnostic Peritoneal Lavage
• Ultrasound
• Arterial Blood gases
• Pulse oximeter and O2 sats
• Urinary / gastric catheters unless
contraindicated– monitor urine output
• ECG

18
 = Full set of VS, Family, Five
interventions

= Give comfort measures

= History taking / Head to toe

= Inspect posterior surfaces

1. Neurologic Assessment:
-LOC, GCS, pupils, motor movement
and strength, AVPU

lert (no need of stimulus to respond)

erbal ( requires verbal stimulus to
respond)
ain ( pain is needed to evoke a
response)
nresponsive to any stimulus
2.
usual history taking + those related
to MVA, Falls, Gunshot wounds,
Penetrating/ stab wounds, SAMPLE

igns and Symptoms,

llergies,
edications,
ast history,
ast food intake,
vents prior to the event
 – Overall
health condition, skin, color,
gait, posture, odors/markings,
mood, affect, VS, O2
saturation.

4.
– remove
clothing
ANSWER WORKSHEET ON TRIAGING