Acute biologic crisis
- Condition that may result to patient mortality if
left unattended in a brief period of time.
- Condition that warrants immediate attention
for the reversal of disease process and
prevention of further morbidity and mortality.
Burns
- Occurs when injury to the tissues of the body is
caused by heat, chemicals, electrical current, or
radiation
- Should be viewed as preventable
- Results in 10-20 thousand deaths annually
- Survival best at 15-45 years old
- Children, elderly , and diabetics
- Survival best burns cover less than 20% of TBA
Influences: burning agents, duration of contact time,
excessive heat, type of tissue that is injured
Types of burn injury
- Thermal burn
- Chemical burn
- Smoke inhalation burn
- Electrical burns
- Cold thermal injury
Thermal burn
- Caused by flame, flash, scald or contact with hot
objects
- Most common type of burn
Chemical burns
- Result from tissue injury and destruction from
acids, alkalis, and organic compound
- Alkali burns are hard to manage because they
cause protein hydrolysis and liquefaction. (it
adheres to the tissue)
- Damage continues after alkali is neutralized
- Can be found in fertilizers, ovens
Radiation
- Result from radiant energy being transferred to
the body resulting in production of cellular
toxins
Electrical Burns
Results for the conversion of electrical energy into heat.
Extent of injury depends on the type of current, the
pathway, of flow, local tissue resistance and duration of
contact.
First-aid: cervical immobilization
Classification of burn injury
 Severity of injury is determined by
- Depth of burn
- Extent of burn in percent of Total Body Surface
Area
- Location of burn
- Patient risk factors
Epidermis- thick as paper, non-living epithelial cells,
provides protective barrier of skin, regulate
body temp, fluid and electrolytes
Depth of burn
- Burns have been defined by degrees (1st, 2nd,
3rd, and 4th)
- ABA advocates categorizing the burn according
to depth of skin destruction. (partial-thickness
burn, full-thickness burn)
1. Superficial partial thickness burn
- Involves the epidermis: reddish intact, skin;
painful
2. Deep Partial Thickness burn
- Destruction of the epidermis
- Involves the dermis; moist surface; with blisters;
painful; red ; shiny ; wet ; severe pain
- Hospitalization required over 25% of body
surface involve
- Takes longer to heal
3. Full thickness burn
- Total destruction of epidermis, dermis,
underlying tissue (fats, muscle, bones)
- Wound color: white, red, brown, black
- Burned areas are painless because nerve fibers
are destroyed
- Not enough skin cell to regenerate
4. Deep full thickness ( 4th degree ) –
- Involves injury to muscles and bone = appears
black (eschars) – hard and inelastic healing
takes weeks to months; grafts are required.
Extent of burns
- Two commonly used guides for determining the
total body surface area
 Lund-Browder chart- considered more
accurate. (age in proportion to body area
size)
 Rule of nine- considered adequate for initial
assessment of adult patients
 Superficial burns are not involved in the
calculation
Lund- browder chart - Macrophages: a type of white blood that ingest
(takes in) foreign material. Macrophages are
key players in the immune response to foreign
invaders such as infectious microorganisms.

Fluid shift
- Occurs after initial vasoconstriction, then
dilation
- Blood vessel dilate and leak fluid into the
interstitial space
- Known as third spacing or capillary leak
syndrome
- Causes decreased blood volume and blood
pressure
- Occurs within the first 12 hours after the burn
and can continue to up to 36 hours.

Fluid imbalances
- Occurs as a result of fluid shift and cell damage
Rule of Nine
- Hypovolemia
- Considered adequate for initial assessment of
adult patients. ( used when no specific age is - Metablic acidosis
given ) - Hyperkalemia
 Head and Neck = 9% - Hyponatremia
 Each upper extremity ( arms ) = 9% ( 4.5%each - Hemoconcentration ( elevated blood osmolality
side ) , hematocrit/ hemoglobin) due to dehydration
 Each lower extremity ( leg ) = 18%
 Anterior trunk = 18% Fluid Remobilization
 Post. Trunk = 18% - Occurs after 24 hours
 Genitalia ( perineum ) =1 % - Capillary leak stops
- See diuretics stage where edema fluid shifts
Baby/ infants from the interstitial spaces into the vascular
 Head and neck = 21% space
 Each arm = 10% - Blood volume
 Back =13% - Increases leading to increased renal blood flow
 Buttocks =5 % and diuresis
 abdomen = 13% - Body weight returns to normal
 Each leg = 13.5 - See hypokalemia
 Genital area = 1%
CURLING’S ULCER
PARKLAND ( BAXTER ) FORMULA for fluid replacement - Acute ulcerative gastro duodenal disease
- 4ml lactated Ringer’s Solution x Kg body mass X - Occur within 24 hours after burn due to
total percentage of body surface burned reduced GI blood flow mucosal damage
- 1st 8 hours = ½ of total hour fluid replacement - Treat clients with h2 blockers, mucoprotectants
- Next 8 hrs = ¼ of total and early enteral nutrition
- Last 8 hrs = ¼ of total - Watch for sudden drop in hemoglobin

VASCULAR CHANGES RESULTING FROM BURN Phase of burn management:

INJURIES
- Circulatory disruption occurs at the burn site
immediately after a burn injury
- Blood flow decreases or ceases due to occluded
blood vessels
- Damaged macrophages within the tissues
release chemicals that causes constriction of
vessels
- Blood vessels thrombosis may occur causing
necrosis
1. Prehospital care- care begins.
2. Emergent (24-48 hrs/resuscitative)
3. Acute (wound healing)- wound care
4. Rehabilitative (restorative)
** Planning begins as soon as formal assessments are
being performed
1. PREHOSPITAL CARE
- removing the source of burn or stopping the
burning process.
- Use cool running water for 15 minutes
 - *10% burn cover with towel and damp it in a
tap water.
- *minor burn 2-4 inches in diameter can be
manage at home
- *more than 10%
- Individuals must be involve to adequately
supply information to medical
At the scene of the injury, priority are….
 Remove the person from the source of the burn
and stop the burning process
 Rescuer must be protected from becoming part
of the incident
Classification of minor burns
 1st and 2nd degree burns – with less than 2-4
inches in diameter can be manage at home
Major Burns
 If the burn is large, more than 10% of the TBSA,
always focus airway, breathing and circulation if
you suspect electrical or inhalation injury
 You may also check for edema... elevate and
foot to decrease pain and swelling
 Large burn should only be cool for not more
than 10 minutes because patient might be at
risk for hypothermia because of extensive heat
loss
 Never cover a burn with ice because of
hypothermia and vasoconstriction
 If there is adherent clothing, just leave in place
until patient is transferred in the hospital and
the patient should be then wrap in a dry sheet
or blanket to prevent contamination of the burn
and provide warmth to the patient
 Chemical burns is best treated by removing
chemical and the affected area should be
flushed by water to irrigate the skin
 Dry chemicals in powered form may be gently
brush off prior to flushing
 Clothing and injury may harbor the chemical
involve (careful removal is needed)
 Patient with inhalation injury must be observe
closely for signs of respiratory distress and
comprise, they need to treated quickly and
efficiently
 Patient with body burn and inhalation injury,
transfer immediately to the nearest hospital or
burn facility
2. EMERGENT PHASE (RESUSCITATIVE PHASE)
- Immediate problem is fluid loss, edema , reduced
blood , flow ( fluid and electrolytes shifts)
- Goal:
1. Secure airway
2. Support circulation by fluid replacement
3. Keep the client comfortable with analgesics
4. Prevent infection through wound care maintain
body temp.
5. Provide emotion support
- Knowledge of circumstances surrounding the burn
injury
- Obtain client’s pre-burn weight ( dry weight) to
calculate the fluid rates
- Calculations based on weight obtained after fluid
replacement is started are not accurate because of
water – induced weight gain
- Height is important determining body surface area (
BSA) which is used to calculate nutritional needs
- Know client’s health history because the physiologic
stress seen with a burn can make latent disease
process develop symptoms.
Client Manifestation in the Emergent Phase
- Clients with major burn injuries and with inhalation
injury are at a risk for respiratory problems
- Inhalation injuries are present in 20% to 50 % of
clients admitted to burn centers
- Assess the respiratory system by inspecting the
mouth, nose , and pharynx
- Burns of the lips , face, ears, necks, eyelids,
eyebrows, and eyelashes are string indicator that an
inhalation injury may be present
- Change in respiratory pattern may indicate a
pulmonary injury.
- The client may : become progressively hoarse,
develop a brassy cough, drool or have difficulty
swallowing, produce expiratory sounds that include
audible wheezes, crowing and stridor
- Upper airway edema and inhalation injury are most
common in the trachea and mainstem bronchi
- Auscultate these area for wheezes
- If wheezes…
- Cardiovascular will begin immediately which can
include shock ( shock is a common cause of death in
the emergent phase in clients with serious injuries)
- Obtain a baseline EKG
- Monitor for edema, measure central and peripheral
pulses, blood pressure, capillary refill and pulse
oximetry
- Changes in renal function are related to decreased
renal blood flow
- Urine is usually highly concentrated and has a high
specific gravity
- Urine output is decreased during the first 24 hours if
the emergent phase
- Fluid resuscitation is provided at the rate needed to
maintain adult urine output at 30 to 50- ml/hr (it is
not the accurate way to know normal urine output; if
the weight is high the output should also be high)
- Measure BUN , creatinine and NA levels.
Clinical Manifestation
1. Sympathetic stimulation during the emergent
phases causes reduced GI motility and paralytic
ileus
2. Auscultate the abdomen to asses bowel sounds
which maybe be reduced
3. Monitor for n/v and abdominal distention
4. Clients with burns of 25% TBSA or who are
intubated generally require a NG tube inserted..
Skin Assessment
1. Assess the skin to determine the size and depth
of burn injury
2. The size of the injury is first estimated in
comparison to the total body surface areas (
 TBSA ). For example , a burn that involves 40% - Removal of exudates and necrotic tissue, cleaning
of the TBSA is a 40% burn the area , stimulating granulation and
3. Use the rule of nice for the client whose weight revascularization and applying dressing.
are in normal proportion to their heights. Debridement may be needed.
IV Fluid Therapy  Wound care
1. Infusion of IV fluids is needed to maintain o Daily observation
sufficient blood volume for normal CO o Assessment
2. Clients with burns involving 15% to 20% of the o Cleansing
TBSA require IV fluid o Debridement
3. Purpose is to prevent shock by maintaining o Dressing application
adequate circulating blood fluid volume o Enzymatic debridement (Maggots therapy)
4. Severe burn requires large fluid loads in a short – Speeds up removal of dead tissue from healthy
time to maintain blood flow to vital organs. wound bed
5. Fluid replacement formulas are calculated from o Appropriate coverage of the graft:
the time of injury and nor from the time of o Gauze next to graft followed by middle and outer
arrival at the hospital dressings
6. Diuretics should not be given to increase urine Dressing the burn wound – should be 3 layers of
output. Change the amount and rate of fluid gauze
administration. Diuretics do not increases CO;
they actually decrease circulating volume and 4. REHABILITATION PHASE
CO y pulling fluid from the circulating blood - Started at the time of admission
volume to enhance diuresis. - Technically begins with wound closure and ends
when the client returns to the highest possible
 Common fluids level of functioning
- Protonate or 5% albumin in isotonic saline ( ½ given - Provide psychosocial support
in first 8 hrs; ½ given in the next 16 hrs) - Assess home environment, financial resources,
- LR without dextrose ( 1.2 given in first 8 hrs; ½ given medical equipments, prosthetics rehab, health
in the next 16 hrs ) teaching should include symptoms of infection
- Crystalloid ( hypertonic saline ) adjust ti maintain drugs regimens, f/u appointments , comfort
urine output at 30 ml/hr measures to reduce pruritus.
- Crystalloid only ( lactated ringers ) Diet
Nursing diagnonsis: decreased CO, deficient fluid volume - Initially NPO
r/t active fluid volume loss, ineffective tissue perfusion, - Begin oral fluid after bowel sounds returns
ineffective breathing pattern - Do not give ice chips or free water lead to
3. ACUTE PHASE electrolyte imbalance
- Lasts until wound closure is complete - High protein, high calorie
- Care is directed towards continued assessment - General diet  soft diet  DAT
and maintenance of the cardiovascular and Goal
respiratory system 1. Prevent complication ( contractures)
- Pneumonia is a concern which can result in 2. Vital signs hourly
respiratory failure requiring mechanical 3. Assess respiratory function
ventilation 4. Tetanus booster
- Infection ( tropical antibiotics – Silvadene) 5. Anti-infective
- Tetanus toxoid 6. Analgesics
- Weight daily without dressing or splints and 7. No aspirin
compare to pre-burn weigh 8. Strict surgical asepsis
- A 2% loss of body weigh indicated a mild deficit 9. Turn q2hr to prevent contractures
- A 10% or greater weight loss requires 10. Emotional support
modification or calorie intake monitor for sign
infection Debridement
- Monitor for signs of infection
- Done with forceps and curved scissors or
 Labs Values through hydrotherapy ( application of water for
1. Na treatment
2. K - Only loose eschar removed
Nursing diagnosis in the acute phase: impaired skin - Blisters are left alone to serve as a protector-
integrity; risk for infection; imbalanced nutrition; controversial
impaired physical mobility; disturbed body image Post Care of Skin Grafts

Planning and Implementation - Maintain dressing

1. Nonsurgical management - Use aseptic technique
- Graft should look pink if it has taken after 5 days
 - Skeletal traction may be used to prevent
contractures
- Elastic bandages maybe apply for 6 months to 1
year to prevent hypertrophic scarring.
MANAGEMENT OF BURNS
1. Administer fluids as prescribed
2. Maintain a high calorie , high protein diet
3. Monitor intake and output
4. Monitor for infections
BURN MEDICATIONS
1. Nitrofurazone ( furacin ) – broad spectrum
antibiotics ointment or cream – used when
bacterial resistance to other drugs is a problem:
apply 1/16 inch thick film directly to burn
2. Mafenide ( sulfamylon ) – water soluble cream
bacteriostatic gr+- bacteria – apply 1/16 inch
directly to burn- notify physician if
hyperventilation occurs as this drug may ppt.
metabolic acidosis.
3. Silver sulfadiazone ( silvadene ) – cream broad
spectrum to gr +-,does not cause metabolic
acidosis : keep burn covered at all times with
sulfadiazone
4. Silver nitrate – antiseptic solution against gr-,
dressings are applied to the burn and then kept
moist with silver nitrate; used on extensive
burns that may precipitate fluid and electrolyte
imbalance.
NCM 106 (Mr. Palomar)
Jan. 17, 2019
PRELIMS
DKA/HHNS
DKA- is a life threatening complication of DM type I=
develops becase of severe insulin deficiency.
- ketosis and metabolic acidosis
- absence or adequate amount of insulin.
- disorder of metabolism (carbhydrates, protein
and fats) metabolic emergency
- insulin dependent client
manifestation
 Hyperglycemia
 dehydration
 electrolyte loss and acidosis (HCO3= below 15
and pH=7.35 and below)
CAUSE: missed insulin dose 20% (inavailability of insulin,
psychological reasons ex. rebellion of authority.) or
infection/illness 40%
PATHOPHYSIOLOGY
the amount of glucose in the body is decrease when
entering the cell, gluconeogenesis, increase the
production of the glucose of the kidney causing
hyperglycemia.
insulin- helps the glucose to enter the cell.
the kidney will excrete glucose along with the fluid,
causing the electrolyte loss- osmotic pressure- polyuria
(excessive urine output) lead to dehydration and
electrolyte loss.
400-500 meq of NA, K.
6.5 L- H2O
== within 24 hours
Insulin deficient- lipolysis (breakdown of fats)
metabolic acidosis
The fats that release ketones
3P’s- the effect of
the glucose is too high, gylsuria
increase hunger- develops if body has difficulty to
response on insulin (insulin difficulty)

DIAGNOSTIC:
Glucose level
BUN Inc- protein intake
Creatinine Inc
hematocrit Inc
ABG- metabolic acidosis
  An ABG test may be most useful when a
INTERVENTION person’s breathing rate is increased or
- management of complication decreased or when the person has very high
- Evaluation therapy blood sugar levels, a severe infection, or heart
- management of dehydration failure

HHNS- SIMILAR TO dka WITH EXTREME hyperglycemia What is an ABGs?

except that in HHNS there is no acidosis. This is for DM  pH- Hydrogen ions shows Acidity or alkainity
type 2.  PCO2- partial pressure co2 –for excretion of the
lungs/ respiratory parameters
Assessment  PO2- partial pressure o2 -Dissolve in the blood/
- 300-800mg/dl blood glucose ability to pick up oxygen in the lungs
- low bicarbonate and low ph  HCO3- bicarbonate (Metabolic parameters-
- dehydration ability to retain bicarbonate)
- mental status changes  BE- base excess
- neurological deficits  SAO2- oxygen saturation
- Seizures
ABG values
NURSING INTERVENTION  pH = 7.35-7.45
 Administer insulin IV push 5-10 units 1st then IV  Paco2 = 35-45 mmHg (respiratory)
infusion  Hco3 = 22-26 meq/L (metabolic)
 restore fluids (Administer fluids as prescribed)  Pao2 = 80-100 mmHg
o Treat dehydration with rapid infusion of  Sao2 = 95-100%
NSS or .45% saline
o when blood glucose reaches 250-300 Equipment: blood gas kit
mg./dl or D5 .45% saline is used  1ml syringe
 23-26 gauge needle
 Always use infusion pump for IV insulin
 Stopper or cap
 Monitor serum potassium (initially as a result of
 Alcohol swap
acidosis hyperkalemia is present upon admin of
 Gloves
insulin K+ level drops)- potassium cling to
 Plastic bag or crashed ice
insulin, causing the decrease of potassium-
 Lidocaine (optional)
releasing of K.
 Vial of heparin (1:1000)
 monitor LOC= to rapid decrease in blood  Par code or label
glucose may cause cerebral edema. ** for syringe, it has heparin (not blood clot)

Arterial Blood Gas (ABG)

- Major function of the pulmonary system (lungs Preparatory phase:
and pulmonary circulation) is to deliver oxygen  Record patient inspired oxygen concentration
to cells and remove carbon dioxide from the  Check patient’s temperature
cells.  Explain the procedure to the patient
- If the patient’s history and physical examination
 Perform Allen’s test
reveal evidence of respiratory dysfunction,
 Provide privacy
diagnostic test will help identify and evaluate
 If not using heparinized syringe, heparinize the
the dysfunction
needle
- ABG analysis one of the first test ordered to
 Wait at east 20 minutes before drawing blood
assess respiratory status because it helps
for ABG after initializing, changing, or
evaluate gas exchange in the lungs
discontinuing oxygen therapy, or settings of
- An ABG test can measure how well the person’s
mechanical ventilation, after suctioning the
lungs and kidneys are working and how will the
patient or after extubation
body is using energy
- It is diagnostic procedure in which a blood is
Allen’s test
obtained from an artery directly by an arterial
- it is a test done to determine hat collateral
puncture or accessed by away of indwelling
circulation is present from the ulnar artery in
arterial catheter
case thrombosis occur in the radial
Indication:
 To obtain information about patient ventilation
(pco2), oxygenation (po2), and acid base balance
 Monitor gas exchange and acid base
abnormalities for patient on mechanical
ventilator or not
 To evaluate response to clinical intervention
and diagnostic evaluation (oxygen therapy)

Sites for obtaining ABG
 Radial artery (most common)
 Brachial Artery
 Femoral Artery
Radial is the most preferable site used because:
- it is easy to access
- it is not a deep artery which facilitate palpation,
stabilization and puncturing
- the artery has a collateral blood circulation
Performance phase:
 Wash hands
 Put on gloves
 Palpate the artery for maximum pulsation
 If radial, perform Allen’s test
 Place a small towel roll under the patient wrist
 Instruct the patient to breath normally during
the test and warn him that he may feel brief
cramping or throbbing aim a the puncture site
 Clean with alcohol swab in circular motion
 Skin and subcutaneous tissue may be infiltrated
with local anesthetic agent id needed
 Insert needle at 45 radial, 60 degrees brachial
and 90 femoral
 Withdraw the needle and apply digital pressure
 Check the bubbles in syringe
 Place the capped syringe in the container of ice
immediately
 Maintain firm pressure on the puncture site for
5 minutes, if patient has coagulation
abnormalities apply pressure for 10-15 minutes
Follow up phase
 Send labeled, iced specimen to the lab
immediately
 Palpate the pulse distal to the puncture site
 Assess for cold hands, numbness, tingling or
discoloration
 Documentation include: result of Allen’s test,
time the sample was drawn, temperature,
puncture site, time pressure was applied and if
O2 therapy is there
 Make sure it’s noted on the slip whether the
patient is breathing room air or oxygen. If
oxygen, document the number of liters. If the
patient is receiving mechanical ventilation, FIO2
should be documented
Potential complications
 Pain
 Hematoma, hemorrhage
 Trauma to vessel
 Distal ischemia
 Numbness
 Arteriospasm
 Air or clotted-blood emboli
 Vasovagal response
 Arterial occlusion
 Infection
A look at acids and bases
- the body constantly works to maintain a
balance (homeostasis) between acids and
bases. Without that balance, cells can’t function
properly. As cells use nutrient to produce the
energy, two by-products are formed H+ and CO2.
Acid-Base balance depends on the regulation of
the free hydrogen ions.
- Even slight imbalance can affect metabolism
and essential body functions. Several conditions
as infection or trauma and medications can
affect acid-base balance
6 easy steps to ABG analysis:
1. Is the pH normal? Dec. 7.35- acidosis; inc. 7.45-
alkalosis
2. Is the CO2 normal? Dec. 35- alkalotic; inc. 45
acidosis
3. Is the HCO3 normal? Same with ph
4. Match the CO2 or the HCO3 with the pH if HCO3
matches with the pH (metabolic); if CO2
matches with the pH (respiratory), if both
matches the pH (mixed)
5. Does the CO2 or the HCO3 go to opposite
direction of the pH? If opposite, then
compensated.
6. Are the PO2 and the O2 saturation normal
ABG values
 pH = 7.35-7.45
 Paco2 = 35-45 mmHg (respiratory)
 Hco3 = 22-26 meq/l (metabolic)
 Pao2 = 80-100 mmHg
 Sao2 = 95-100%
Step1: analyze the pH
- The first step in analyzing ABGs is to look at the
pH. Normal blood pH is 7.4. plus, or minus 0.05,
forming the range 7.35 to 7.45. if the blood pH
falls below 7.35 it is acidic. If blood pH rises
above 7.45 it is alkalotic.
Step 2: Analyze the CO2
- Below 35 is alkalotic; above 45 is acidic
Step 3: analyze the HCO3 (same with pH)
- If the HCO3 is below 22, acidotic. If above, 26;
alkalotic
Step 4: match the CO2 or the HCO3 with the pH
- If the pH is acidotic, and the CO2is acidotic,
then the acid base disturbance is being caused
by respiratory system. Therefore, we call it
respiratory acidosis. If the pH is alkalotic and
the HCO3 is alkalotic, is is more on metabolic or
renal system. Therefore, metabolic alkalosis

Step 5: does the CO2 or HCO3 go tot the opposite
direction of pH
- If so (opposite side), there is compensation by
the system. EXAMPLE. pH is acidotic, the CO2
acidotic and the HCO3 is alkalotic, then it is
respiratory acidosis, and HCO3 is alkalotic. The
Co2 matches the pH making acid-bas disorder.
Step 6: analyze the PO2 and O2 saturation
- If they are below normal, there is evidence of
hypoxemia (PaO2)
- Hypoxic – No O2 Therapy
- Hypoxemic- With intervention
metabolic alkalosis – vomiting
*If pH is normal, HCO3 and PaCO2 are abnormal  Fully
Compensated
*If pH is abnormal and HCO3 and PaCO2 are abnormal 
Partially compensated
*If pH is abnormal, either HCO3 or PaCO2 is normal 
Uncompensated
Acute Respiratory Failure
Respiratory Function
 Oxygen transport
 Oxygen supplied to and carbon dioxide is
removed from cells by way of circulating
blood
 Respiration
 The whole process of gas exchange
between the atmospheric air and blood and
between the blood and cells of the body
 Ventilation
 Physical factor that govern air flow in and
out of the lungs
Ventilation
 Physical factors that govern airflow in the lungs
a) Air pressure variances
b) Airway resistance
c) Compliance
Ventilation – Air pressure variances
 Air flows from a region of higher pressure to a
region of lower pressure
 During inspiration, movement of the diaphragm and
other muscles of respiration enlarges the thoracic
cavity and thereby lowers the pressure inside the
thorax to a level below that of atmospheric
pressure
 Air is drawn to the trachea and alveoli
 During expiration, the diaphragm relaxes and the
lungs recoil, resulting in a decrease in the size of
thoracic cavity
 The alveolar pressure then exceeds the atmospheric
pressure, and air flows from the lungs into the
atmosphere
Ventilation – Airway resistance
 Resistance is determined by the radius or size of the
airway through which the air is flowing
 Any process that changes the bronchial diameter of
width affects airway resistance and alters the rate
airflow for a given pressure gradient
Ventilation – Compliance
 A measure of elasticity, expandability, and
distensibility of the lungs and thoracic structures
If the respiratory system fails:
 Blood will not be oxygenated
 Co2 will not be removed
Respiratory failure
Defined as:
 PaO2 < 50 mmHg (hypoxemia)
 PaCO2 > 50 mmHg (hypercapnia)
 pH < 7.35
Respiratory failure
 Exists when the exchange of oxygen for carbon
dioxide in the lungs cannot keep up with the
rate of oxygen consumption and the carbon
dioxide production by the cells of the body
2 classification of Respiratory Failure:
1. Acute Respiratory failure – sudden and life-
threatening deterioration of gas exchange function
of the lung
2. Chronic respiratory failure – deterioration in the gas
exchange function of the lung that has developed
insidiously or has persisted for a long period after
an episode of ARF
Causes of Respiratory Failure:
1. Decreased respiratory drive
 Impairment in the response of
chemoreceptors in the brain to normal
respiratory stimulation
 Examples:
Severe brain injury
Large lesion in the brainstem
(multiple sclerosis)
2. Dysfunction of chest wall
 Any disease or disorders in the nerves,
spinal cord, muscles or neuromuscular
junction involved in respiration seriously
affects ventilation
 Examples:
Myasthenia gravis, poliomyelitis,
peripheral nerve disorders,
amyotropic lateral sclerosis,
Guillain-Barre syndrome and
cervical and spinal cord injuries
3. Dysfunction of lung parenchyma
 Examples
- Pleural effusion- fluid in lungs
- Hemothorax- presence of blood
- Pneumothorax- presence of air
- Pneumonia- infection
- Status asthmaticus
- Lobar atelectasis- lobes can rupture
 - Pulmonary edema- swelling Medical management:
 Intubation
4. Other causes  Mechanical ventilation
 Post surgery (major thoracic, cardiac and
abdominal surgery) Hypoxemia – is the major immediate threat to organ
 Effects of anesthetic agents, analgesics, function. Therefore, the first objective in the
sedatives that may depress respiration management of respiratory failure is to reverse and/or
prevent tissue hypoxia
Types of Acute Respiratory Failure
 Type I – Hypoxemia with normocapnia or Appropriate management of the underlying disease
hypocapnia obviously is an important component in the
 Characterized by a PaO2 of less than 50 management of respiratory failure
mmHg with a normal or low PaCO2
 The most common form of respiratory A patient with acute respiratory failure generally should
failure associated with virtually all acute be admitted to a respiratory care or intensive care unit.
diseases of the lung, which generally involve
fluid filling or collapse of alveolar units Nursing management:
 Pulmonary edema, pneumonia, and  Assisting with intubation and maintaining
pulmonary hemorrhage mechanical ventilation
 Assessment of respiratory status (patient’s level
 Type II – Hypercapnia of response, ABG, pulse oximetry, vital signs
 Characterized by a PaO2 of more than 50 and respiratory system
mmHg  Turning schedule, mouth care, skin care, range
 Common etiologies include: of motion extremities
 Drug overdose, neuromuscular  Assess the knowledge and understanding of
disease disorder and provide health teachings
 Chest wall abnormalities, and
severe airway disorders (asthma, Nursing Diagnosis:
COPD)  Impaired gas exchange (Ventillation-Perfusion-
ABG Result)
 Type III – Combination of two or perioperative  Ineffective airway clearance (Underlying
 Predominantly the result of atelectasis Conditions- Sputum Exam)
 Ineffective breathing pattern (Impaired gas
 Type IV – Circulatory collapse exchange and Ineffective airway clearance-
 Seen in patients who are in shock or in Respiratory Rate)
hypo-perfusion states, without associated  Risk of fluid volume imbalance (Respiratory
pulmonary problems Failure)
 Anxiety
Clinical manifestations:  Imbalance nutrition: less than body
 Restlessness requirements
 Fatigue
 Headache Planning: overall goals
 Dyspnea: special CM  ABG values within patient’s baseline
 Air hunger  Breath sounds within patient’s baseline
 Tachycardia: early sign  No dyspnea or breathing pattern
 Increase BP: early sign  Effective cough and ability to clear secretion
 Use of accessory muscles
 Cyanosis: late sign Prevention
 Consequences of hypoxemia and hypoxia: - Thorough history and physical assessment to
metabolic acidosis and cell death. Decreased identify at-risk patients
cardiac output. Impaired renal function - Early recognition of respiratory distress
 Special CM: tripod position, rapid shallow
breathing pattern
Nursing and Collaborative Management
As hypoxemia progresses: Intervention:
 Confusion  Oxygen therapy: Delivery system should:
 Lethargy o Be tolerated by the patient
 Tachycardia o Maintain PaO2 at 55 to 60 mmHg or
 Tachypnea more and Sao2 at 90% or more at the
 Central cyanosis lowest O2 concentration possible
 Diaphoresis  Mobilization of secretion
 Respiratory arrest o Chest physical therapy
o Hydration
 o airway suctioning
o effective coughing and positioning
 Positive pressure ventilation (PPV)
 Noninvasive PPV
o BiPAP (Bilevel positive airway pressure)
o CPAP (continuous positive airway
pressure) –for patient suffering ARF.
Pressurized air to prevent the throat
muscle from collapsing.
Drug therapy
 Relief of bronchospasm: Bronchodilators
 Reduction of airway formation: corticosteroids
 Reduction of pulmonary congestion: Diuretics,
nitrates if heart failure present
 Anxiolytics: narcotics and benzodiazepine
 IV antibiotics
Physiologic aging resulting:
- Decrease Ventilation
- Allveolar dilation
- Larger air spaces
- Loss of surface area
- Diminished elastic recoil
- Decrease respiratory muscle strength
- Decreased Chest Wall compliance
- Life smoking
- Poor nutritional status
- Less available physiologic reserve
o Cardiovascular
o Respiratory
o Autonomic nervous system
Weaning
 Predictors of successful
- A vital capacity of at at least 15mL/kg of body
weight;
- A negative inspiratory pressure of less than 30
cm
- In the clinical practice additional parameters
such as minutes volume, oxygenation , mean
arterial pressure , arterial pH, and work of
breathing may also be used.
- Standard weaning parameters are less helpful
with patients requiring long- term mechanical
ventilation
- Many studies ( burns at a;., 1995 ) indicate that
the use of a variety of indicators maybe
necessary
- Burns, Burns, and Truwit ( 1994) reviewed and
compared five weaning scales that can be used.
Mechanical ventilation
 Patients with acute respiratory failure
frequently require intubation and mechanical
ventilation
 Important to minimize due to:
Complications:
1. Infection
2. Problems associated with positive pressure
3. Alterations related to endotracheal intubation
4. Loss of verbal communication
5. Positive pressure .
increased pressure levels can results the
following :
- Barotrauma, which may be manifested as
pneumothrorax, pneumomediastinum ( air , in
the mediastinal space ), or subcutaneous
emphysema.
- Positive pressure – hampers the venous return
and can cause a decreased in cardiac output,
urine output  decreased renal perfusion 
increase ADH secretions leading to fluid
retention then lead to edema
- Decrease venour return associated pp may
stimulate osmoreceptors in hypothalamus
decrease in ADH secretion may result to renal
retention.
 Complication related to intubation mechanical
complication related to presences of ETT
 Ventilator induced injury
 Complication related oxygen infectious
complication of mechanical ventilation
Conclusions:
- As patients requiring mechanical ventilation
move beyond the acute unstable phase of their
illness, they no longer require intensive
monitoring and management.
- Specialty units or general medical-surgical floors
are often able to provide care to these stable
patients which focuses on rehabilitation and
weaning from the ventilator.
- An understanding of the reasons for prolonged
mechanical ventilation is necessary for each
patient and the type of ventilation used helps
the nurse establish realistic goals for the
treatment and care of individual patients
- Using physical, nutritional and ventilator
assessment techniques helps identify nursing
interventions and plan care to meet the goals
identified.
- as weaning and rehabilitation progress,
avoiding complications or identifying early
 signs and symptoms of complications will
help prevent extended hospitalization
- Recovery of stable patients needing
prolonged mechanical ventilation may
depend on their nurses’ knowledge, skill and
individualized interventions to help them set
and achieve goal.
 Overfeeding can contribute to:
Fluid overload , glucose intolerance, will
contribute to hypophospothemia
 Pulmonary aspiration ( most dangerous ) assist
overfeeding, silent aspiration
- Bed should be kept at 45 degrees to prevent it,
check feeding tube, peg tube ( no air ) , because
it is directly to the stomach
 Before feeding check for residual content
 Malnutrition
COR PULMONALE
- It is the hypertrophy of the right ventricle
resulting from disease affecting the function
and/or structure of the lung, except when these
pulmonary alterations are the results of disease
that primarily affects the left side of the heart
- It is the enlargement of the right ventricle
secondary to diseases of the lungs, thorax or
pulmonary circulation. Pulmonary hypertension
is usually a preexisting condition in the
individual with Cor pulmonale. COPD is the
most common cause.
- It is a condition in which the right ventricle of
the heart enlarges ( with or without right sided
heart failure) as a result of disease that affects
the structure or function of the lungs ir its
vasculature
Clinical manifestation:
• Dyspnea
• Chronic productive cough
• Wheezing respirations
• Retrosternal or substernal pain
• Fatigue- poor circulation
• Polycythemia (increase amount of hemoglobin)
–poor circulation
o If heart failure accompanies Cor Pulmonale
additional manifestations such as
• Peripheral edema
• Weight gain
• Distended neck veins
• Full bounding pulse
• Enlarged liver
• Palpitation
• Atypical chest pain
• Swelling or the lower extremities (Pitting
associated to hypercapnia)
• Dizziness and even syncope
Diagnosis
• Lab test
• ABG analysis
• Brain natriuretic Peptide - peptide hormones
that is release in response to volume expansion and
increase in the wall (if there is stress in the wall) = helps
in promoting diuresis.
• Pulmonary function test
o to find out the ventilation perfusion
o For anesthesia
• Chest radiography- shows enlargement of the
peripheral lung field
Medical management
 Oxygen therapy - for patients with hypoxemia.
The oxygen will improve hypoxic
vasoconstriction. Oxygen also may improve
pulmonary artery pressure and pulmonary
vascular resistance and polycythemia
associated with hypoxia
 Pharmacotherapy
- Diuretic agents
- Vasodilators
- Beta selective agonists
- Cardiac
- Glycosides
- Theophylline
- Warfarin
 Phlebotomy- for vascular resistance and
decrease pulmonary artery pressure.
Indication for polycythemia vera (hematocrit
is above 65%)
Nursing diagnosis
 Decreased cardiac output related to restricted
cardiac muscle contractility as evidenced by
echocardiography finding
 Impaired gas exchange related to expiratory
airflow obstruction as evidence by decreased
oxygen saturating level
 Impaired tissue perfusion related to deceased
cardiac contractility and expiratory airflow
obstruction as evidence by increased
capillary refilling time >3 sec.
 Activity intolerance related to decreased
cardiac activity and labored respiration as
evidenced by difficulty in performing
activities of daily living (labored respiration)
 Fatigue related to decreased cardiac activity
and labored respirations as evidenced by
difficulty in performing in activities of daily
living
 Anxiety related to breathlessness as
evidences by patient’s verbalization and facial
expressions.
 Imbalance nutrition: less than body
requirement related to breathlessness as
evidenced by weight loss of 10% of kilog per
body weight
 Disturbed sleep pattern related to shortness
of breath as evidenced by presence of dark
circles around the eyes
Nursing management
 Listen to patient’s fears and concerns about
his illness
 Plan a nutritious diet carefully with the
patient and the staff dietitian
  Prevent fluid retention by limiting the
patient’s fluid intake to 1,000 to 2,000 ml
daily and providing a low sodium diet.
 Reposition the bedridden patient often to
prevent atelectasis
 Provide meticulous respiratory care,
including oxygen therapy and for COPD
patients
 Pace patient care activities to avoid patient
fatigue
 Monitor serum potassium levels closely if the
patient takes a diuretic
 Be alert for complaints that signal digoxin
toxicity such as anorexia, nausea, vomiting
and seeing a yellow halo around an object
 Measure ABG levels and watch for signs of
respiratory failure as change in pulse rate,
deep labored respirations, and increased
fatigue produced by exertion
 Instruct patient to schedule frequent rest
periods and to perform his breathing
exercises regularly (for lung expansion and to
prevent atelectasis)
COPD COR PULMONALE
- may involve chronic inflammation and
obstruction of the pulmonary airways with
excess mucus production that causes
obstruction and a mismatch of ventilation and
perfusion
- the alveolar tissue is destroyed along with a
loss in the elastic fibers which impairs the
expiratory phase. This loss also increases air
trapping and collapse of the airway structures
- this is seen in the arterial blood gases as a
decreased PO2 and an increased PCO2.
What is Cor pulmonale in the COPD patient
- the progress of COPD results in right sided
heart failure. The right ventricle has become
hypertrophied and dilated and its function
has become compromised due to pulmonary
hypertension associated with COPD
COPD to Cor pulmonale
- the chronic inflammation and hypoventilation
causes the pulmonary vasoconstriction and
signals the kidney to release erythropoietin in
response to the low oxygen levels
- this in turn stimulates the bone marrow to
produce reticulocytes which are released into
the blood stream to become erythrocytes
- because of the chronic low oxygen levels this
process is continually occurring causing an
excess of red blood cells (polycythemia)
- the progression of COPD results in chronic
hypoxic pulmonary vasoconstriction,
polycythemia, impaired gas exchange
secondary to mucous overproduction and air
trapping which destroys the pulmonary
vascular bed because of decreased oxygen
supply
- the progression leads to pulmonary
hypertension; which puts a stress on the right
ventricle causing it to distend and
hypertrophy
- hypertrophy to the right ventricle is known as
Cor pulmonale
Clinical presentation of the cor pulmonale patient
 most of the symptoms of cor pulmonale are
not often recognize…….
Clinical examination
 the patient has jugular venous distension
 bilateral lower extremity pitting edema
 the patient uses home oxygen at 2L/nasal
cannula at bedtime
 the patients resting pulse oximeter reading is
90% on room air
 a holosystolic murmur at the left lower
sternal border characteristics of tricuspid
insufficiency
 right upper quadrant discomfort upon
palpation
 the patient complains of exertional dyspnea
and fatigue despite use of albuterol inhaler
and pulmicort inhaler.
Pulmonary hypertension causes right sided heart
failure and is charterized by:
1. Jugular vein distension
2. Peripheral edema of legs and ankle
3. Right upper quadrat pain from hepatic
congestion (Hepatomegaly)
Diagnostic Test
 Chest radiography- show enraged pulmonary
artery due to pulmonary hypertension. The
lateral view would show a loss of retrosternal
air spaces due to the enlargement of the right
ventricle
 ECG- show a right bundle branch block and
right axis deviation because of the right
ventricle hypertrophy and atrial enlargement.
(there will be dominant R waves in V1 and V2
and prominent S waves in V5 and V6 because
of right ventricular hypertrophy. Increased P
wave amplitude in lead II due to right atrial
enlargement)
 Echocardiogram- show right ventricular
hypertrophy, right ventricular dilation and
tricuspid regurgitation due to right atrial
enlargement
 Pulmonary function test- indicate impaired
diffusion capacity due to acidotic pH.
 Right Heart Catheterization (GOLD
STANDARD)- patient who present with chest
pain and has nondiagnostic or normal results
of the chest radiograph, echocardiogram, ecg
and pulmonary function test to confirm the
Cor pulmonale.
3 physiological goals for cor pulmonale treatment
 1. Reduce the right ventricular after load
causing a reduction of the pulmonary artery
pressure
2. Decrease right ventricular pressure
3. Improve the contractility of the right ventricle
Treatment
 Oxygen therapy for patients with
hypoxemia. The oxygen will improve hypoxic
vasoconstriction. Oxygen also may improve
pulmonary artery pressure and pulmonary
vascular resistance and polycythemia
associated with hypoxia
 Diuretic Therapy to improve right
ventricular function due to increased right
ventricular pressure. It must be used carefully
because cor pulmonale patients are preload
dependent and under filling of the right
ventricle may decrease the stroke volume and
increase their symptoms. May also increase
the patients risk of developing arrhythmias
and metabolic acidosis of the loss of
potassium form the diuretic
 Inotropic agents are used to increase right
ventricular contractility and decrease the
right ventricle afterload by inducing
pulmonary vasodilation
COPD is the 4th leading cause of death in US. COPD
leads to cor pulmonale. Nurse practitioners will be
expected to manage the treatment of patients with
cor pulmonale. The management will focus the extent
of lung disease and failure.
MIDTERMS
02.12.19
Myocardial infarction “ brain attack”
Primary methods that are used initially to
diagnose MI:
1) ECG ( 12 leads )
- ST segment elevation
2) Patient’s history
Management
 Early management: aspirin is give in
160mL- 325( chew )
 Patient should be in condition cardiac
monitoring
 You have to get serial ECG
 Patient should be given oxygen 0.5 lpm
via nasal cannula ( because of the Clot )
 For chest pain give nitroglycerin
(sublingual) check for blood pressure first
- Hold sublingual meds if BP is 90 or less
than ( systole )
 Don’t give nitroglycerine if HR is less than
50 or higher than 100
 Give morphine sulfate
Thrombolytic drugs- provides maximal benefits/
effect within the first 3- 12 hours after the onset
of the symptoms.
- Converts plasminogen to plasmine
- Should not be given to patient who had
stroke within the year
- Should be given to patient with severe
uncontrolled hypertension
(180/110mmHg)
PTCA (primary percutaneous transluminal
coronary angioplasty)
– is a very invasive procedure
 For patient with PTCA, should be
monitored after procedure for
complication = any evidences of bleeding
Intensive and Immediate Management:
1. Do not give prophylactic dysthymic drugs
within 24 hours
2. Continue nitroglycerine for 2 days
3. Daily aspirin should be continue on in
definite basis
4. Give Flavix if patient is intolerant to
aspirin
5. Beta blockers : should be within initial
hours of infraction can be shifted to,
6. Oral therapy provided without
complication
7. Beta blockers – reduce oxygen demand by
decreasing the heart rate and contractility
8. Calcium channel blocker – standby if the
beta blockers is contraindicated or
ineffective
9. ACE ( angiotensin converting enzyme ) –
administered to patient with MI in interior
wall and with heart failure, it helps prevents
dilation to preserve ejection traction
10. Heparin : given to patient undergoing…
and who are receiving
11. MI patient who has severe congestive
heart failure and pulmonary edema
Complication
 Vascular complication
a. Ischemia and infarction
 Mechanical complication
 Myocardial complication
a. Hypertention
 Pericardium complication
 Thromboembolic complication
- Thrombosis , DVP , pulmonary embolic
 Electrical complication – pacing of ECG ,
VTAC ( ventricular tachycardia – more
than 15bpms )
 Ventricular complication
- Ventricular fibrillation
- SVT
- Atrioventricular block
Nursing diagnosis:
1) Acute pain related to imbalance of oxygen
supply and demand
2) Anxiety related to chest pain , fear of
death , threatening environment
3) Activity intolerance related to ..
4) Risk for injury, bleeding or hemorrhage
related to dissolution of protective clots
Nursing intervention
1) start IV therapy
2) Attachment of electrodes for continuous
cardiac monitoring
3) Encourage DBE- may decrease
dysthymias by allowing the heart to
become less ischemic
4) Maintain O2 stat of > than atleast 92%
5) Offer reassurance and support
6) Relief of pain
7) Provide nitroglycerine sublingual- check
and recheck vital signs every 10 – 15 mins
8) Opioids: morphine ( caution because it
decreased BP and HR )
9) Give nitroglycerine as prescribed
10)Supine position to maintain hypertension
STROKE
- Is sudden loss of brain function due to a
disruption in the brain
Two categories :
1) Hemorrhagic (15%)
2) Non – hemorrhagic (85%)
Cause of stroke :
A. Embolism – from the thrombus outside
the brain
B. Thrombosis – occlusion of the blood flow
C. Hemorrhage- due to rupture aneurysm,
due to high blood pressure , trauma , or
any hemorrhagic disorders
- The underlying cause of stroke is OXYGEN
AND NUTRITON DEPREVIATION
Ischemic Stroke
-caused by embolic and thrombosis
- Left is right , right is left
Signs and symptoms:
A. Numbness
B. Blurring of vision
C. Sudden and severe headache without
known cause
D. Slurring of speech
Diagnostic test
1) CT Scan
2) Angiography
3) Brain scan
4) Carotid duplex test – shows blood flow in
carotid arteries
5) MRI
6) Lab test : NONE
- Some of the test that are used to
establish: blood glucose test ( shows if it
related to hypoglycemia) , hemoglobin
and hematocrit( severe occlusion) Test ,
PTT, PT ,
Management :
1) Thrombolytic therapy
2) Aspirin- prevent ischemic stroke
3) Anti-hypertensive and anti-arrhythmic
4) Anti-inflammatory and corticosteroids-
prevents cerebral edema
5) Analgesics is given
6) Mannitol an or anti-edema – for brain
edema
Surgical treatment
1) Craniotomy – depends on the extent of
stroke – to remove hematoma
2) Carotid endarectomy – removal of the
3) Extra cranial bypass – for stenosis ,
underpass or overpass
Hemorrhagic Stroke – Bleeding that occurs at any
parts of the brain, usually at subarachnoid, SAH
space
- Usually the cerebrospinal fluid should
occupy this space
Cerebral aneurysm – weakness of the wall of the
cerebral artery
Berry Aneurysm – sack like pouching
Arises at the arterial area of Bundle of His, circular
stenosis
Major cause: rupture of cerebral aneurysm
- Congenital defects
Nursing diagnosis
 (SAH) subarachnoid hemorrhage
 Cerebral aneurysm
- Berry aneurysm: most common type of
aneurysm
Common cause: trauma
Signs and symptoms
- Hematoma due to blood oozing
- Stiff back and legs
Rupture occurs abruptly;
Signs and symptoms
- Sudden severe headache due to bleeding
- Projectile vomiting
- Altered LOC including coma
- Meningal irritation
o Seizure (meningitis)
o Irritability
- Diplopia, inability to rotate the eye, because
of compression of occulomotor nerve
Grading of Bleeding INCREASED INTRACRANIAL PRESSURE
1- Rigid: 75ml of blood and 75 cerebro fluid
2 – minimal to mild: same with 1 but there is nerve Cerebral blood flow: matches the local metabolic of
palsy the brain
3- moderate: confused, drowsy plus 1 and 2 and CPP: Normal: to perfuse the cells of the brain 70-
mild vocal deficit 90
4- severe bleeding: stuporous, and 1 2 3 symptoms ICP measured in the lateral ventricles
5 – fatal :moribu Normal: 1-15 mmHg / 60-100 ml
Injured brain: CPP more than 70
Diagnostic test
- Cerebral angiography MONRO KELLIE HYPOTHESIS
- CT scan - Bc of the limited space of expansion
- Lumbar Puncture- analysis of cerebrospinal between the skull so the increase of any
fluid components causes a change in the volume
- MRI – brain spasm and location of bleeding of others
- Components compensate each other,
Surgical repair accomplished by: displacing or shifting of
- Clipping CSF, decrease cerebral blood volume
- Ligating
- Wrapping the aneurysm neck w muscles Cerebral response to increase ICP: Cushing’s
- Intentional geology with endovascular Triad: increase BP, HTN, Bradycardia,
balloon therapy Bradypnea, requires emergent intervention

Non surgical Why monitor? Decrease diuretic that can cause

- Electro thrombosis Diabetes Insipedus
- Bed rest for 46 minutes, Head of the bed Management
- Manage edema
should only 30
- Lower CSF vol
- Avoid stimulants, caffeine
- Decrease cerebral blood vol
- Administer analgesics, antihypertensive,
- Restrict fluids
coticostreroids, Phenobarbital,
vasoconstrictors In general, the management is PCO2 should
- Mechanical Ventilation maintain 35 to 45, px on stroke avoid hypoxia,
- Cardiac monitoring intubation
- Position to promote pulmonary drainage ICP : elevate head of bed
Continuous ECG
Aneurysm precaution
- Bed rest
- Limit visitors
- Limit coffee and physical activity
- Loc and VS
- Avoid rectal temp (vagus nerve)
- Acute measure
- WO danger signs that indicate enlarging
aneurysm : Decrease Loc, unilateral pupil,
onset of worsening hemopheresis, BP is
high PR is low, sudden onset headache,
projectile vomiting
- VASOSPASM (one thing to WO) motor
focal deficit, worsening headache
o Hypervolemic, hemodilusion
o Administer normal or hypertonic
saline
o Blood product (whole blood) Pack
RBC
o Albumin
o Crystaloid solution

Meds
- Calcium channel Blockers