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m Care given to patients who are suffering and

undergoing life-threatening illness or injury.


m Ôhock
m Burn
m Heart failure
m Renal failure
m Diabetic ketoacidosis
m Hepatic coma
m Multiple organ dysfunction syndrome
 !erfussion of the body¶s organs and tissues is
inadequate to meet the oxygen and nutritional demands
of the cells.
m  stages of shock
 st stage (reversible)
 2nd stage compensatory stage of shock
 3rd stage progressive stage of shock (irreversible)
 th stage refractory stage of shock
st stage (reversible) Neutralizes newly acidic
might have no signs at all state

Increase contractility of
Changes in cells due to the heart, increase B!,
Increase ventilation increase heart rate,
decreased perfusion and
oxygen increase delivery of
oxygen to the heart

Anarobic metabolism 2nd stage Neural and Hormonal


(increase in formation of Compensatory stage of Compensatory
lactic acid shock Mechanism
m Baroreceptor reflex
m Central Nervous system ischemic response
m Reflex vanoconstriction
m Ôtimulation of chemoreceptor
‡ Ôtimulates sympathetic
vasoconstrictor fibers
Baroreceptoa
re stimulated ‡ Blood are shunted away
from nonpriority organs to
major organs

Decreasing ‡ vasomotor center becomes


B! or CNÔ ischemic results to Inc CO2
decreasing ischemic
response ‡ Inc CO2 stimulates
MA! vasoconstriction

‡ stimulates the
chemorecept vasomotorcenter
ors
‡ stimulates vasoconstriction
m Norepinephrine-Epinephrine Vasoconstrictor
mechanism
m Renin-Angiotensin Ôystem Activation
m Antidiuretic Hormone
m Release of Glucocorticoids
Adrenal ‡ Norepinephrine as potent
medulla vasoconstrictor
releases
stress ‡ Epinephrine cardiac
hormones stimulant and bronchodilator

Decreasing ‡ stimulated by the


B! or Renin- juxtaglomerular cell
angiotensin ‡ renin convertion to
decreasing system angiotensin I to angiotensin
Map II

‡ osmoreceptors at the
Antidiuretic hypothalamus stimtulates
hormone post. !G to release ADH
‡ ADH retain water.
Compensatory mechanism can no longer
3rd stage
maintain balance
!rogressive stage of shock
Death

Continued anarobic metabolism Increased metabolic acidosis


m Hypovolemic shock
 ^oss of intravascular blood volume.
 Internal fluid shifts
˜ ^ong, closed bone fractures, ruptured spleen, ascites
 External fluid losses
˜ External hemorrhage, excessive gastrointestinal losses,
excessive diuresis.
m Cardiogenic shock
 uhe heart had been damaged so much that it is unable to
supply enough blood to the organs of the body.
 MI, bradycardia
m Anaphylactic shock
 Ôevere and whole-body allergic reaction
 After being exposed to drug,food and insect bite
m Ôeptic shock
 A serious condition that occurs in overwhelming condition
of infection leads to life-treathing low blood pressure.
˜ Meningococcemia
˜ Disseminated intravascular coagulation
 Occurs to in the very old and very young and those who
have other illness.
m Neurogenic shock
 Happens to people with spinal cord injuries or diseases
above the midthoracic region.
m Anaphylactic shock
 Abdominal pain
 Abnormal breathing sound, wheezing
 Anxiety, confusion
 Cough, difficulty of breathing
 Diarrhea
 Dizziness, fainting
 Hives, itchiness
 !alpitation
 Ôkin redness
m Ôeptic shock
 High or very low temperature, chills
 Cool, pale skin
 Rapid pulse
 !alpitations
m Hypovolemic shock
 Anxiety
 Confusion
 Cold, clammy skin
 Decreased or no urine output
 Weakeness
 !ale skin color
 Rapid breathing
 Ôweating
m Cardiogenic shock
 !erfused sweating
 Rapid pulse
 Restlessness, agitation and confusion
 Agitation
 Ôhortness of breath
 Ôkin discoloration
m Neurologic
^ow B!
Decreased urine output
Decreased peripheral pulses and capillary refill
Change in respiratory patterns
m Cardiogenic shock
 Coronary angiography
 Echocardiogram
 Electorcardiogram
 Blood chemistry
 CBC
m Hypovolemic shock
 Ôwan-Ganz right heart catheterization
 Urinary catheterization
m Anaphylatic shock
 Ôkin test
m Ôeptic shock
 Blood works and culture and sensitivity test
 Urinalysis
 Chest x-ray
m Neurologic
 Cu scan
 X-ray
m Hypovolemic
 Ñeep patient warm
 Ñeep flat on bed with leg elevated 2 inches to increase
circulation
 Do not give fluids by mouth
 Ôtabelize the patient before moving
m Cardiogenic
 Medication to increase cardiac rate and B!
˜ Dopamine
˜ Dobutamine
˜ Ephineprine
˜ Norephineprine
 Electric shock therapy
 !acemaker implantation
 IV fluids
m Anaphylaxis
 B^Ô
 Endotreacheal intubation or tracheostomy
 Ephineprine
 IV fluids
 Antihistamines
m Ôeptic shock
 Mechanical ventilator
 Drugs to treat low B!, infection and blood clotting
 IV therapy
 Oxygen
 Ôurgery
m Neurogenic
 Ôtabilizaion of the spinal cord,surgery
 Establish airway
 Mechanical ventilator, with !EE! (pulmonary end-
expiratory pressure)
 Ôodium bicarbonate
m Hypovolemic
 èluid volume deficit
 Altered tissue perfusion, peripheral
 Decreased cardiac output
 Anxiety and fear
 Ineffective family coping
 Ñnowledge deficit
 Altered nutritiion, less than body requirement
m Cardiogenic
 Decreased cardiac output
 Altered tissue perfusion, myocardial
 Altered tissue perfusion, peripheral
 Impaired gas exchange
 èluid volume excess
 Anxiety and fear
m Ôeptic
 Ineffective thermoregulation
m Anaphylactic
 Ineffective breathing pattern
 Risk for impaired skin integrity
m Neurogenic
 Hypothermia
m Ôkin
 Important to the fluid and temperature regulation of the
body.
 !rotective barrier againts bacteria and viruses
 Have 3 parts
˜ Epidermis
˜ Dermis
˜ Ôubcutaneous
m èirst degree (superficial thickness)
 Ôuperficial and cause local inflammation
 !ain, redness and mild amount of swelling
m Ôecond degree (superficial partial thickness)
 Much deeper with blister formation
m uhird degree (deep partial thickness)
 Deep dermis, reduced sensation
m èourth degree (full thickness)
 Involving all layers of the skin
 Nerve and blood vessels are damaged, this burn appears
white and leathery and painless.
m Burn is not static and may mature
m Inflammation and fluid accumulation in and around
the wound occurs.
m Only the epidermis has the ability to regenerate.
m If the burn involves the face, nose, mouth and
neck, airway might get compromised.
m Chest burn might limit motion of chest during
breathing.
m Burned body area with flexion creases(like the
hand, back of the knee) might lose full range of
motion.
m Burns are measured as a percentage of total body
area affected
m uBÔA involvement
 Burns >20%-25% uBÔA requires IV fluids, for shock may
occur
 Burns >30%-0% uBÔA may be fatal without treatment
m Chemical burn
 Acids and bases
˜ Ôilver nitrate, sulfuric acid, sodium hydroxide
m Electrical burn
 Electric shock due to electric current
 ^ightning strike
m Radiation burn
 Exposure to UV light
m Ôcalding
 Caused by hot liquid or steam
m Emergent phase
 Includes pre-emergency and emergency room care and begins
at the time of injury till the restoration of capillary permeability.
 Usually  -72 hours following burn injury
 uhe management is to prevent hypovolemic shock and
preserve vital organ functioning.
 Hyperkalaemia, hyponatraemia
m Resuscitative phase
 Begins in the initiation of fluids until capillary integrity returns to
normal levels.
 Management in this phase is to prevent shock by maintaining
adequate blood circulating volume.
m Acute phase
 Begins when the patient is hemodynamically stage,
capillary permeability is restored and diuresis has begun
until wound closure is achieved.
 Usually  -72 hours after injury
 Management in this phase focus on infection control,
wound care, wound closure, nutritional support, pain
management and !u.
m Rehabilitative phase
 èinal phase of management of burns
 èocuses that the patient can gain independence and
achieve maximal function.
m 3 phases of scar formation
 st phase that last for a week, body begins to remove
dead cells and fights infection
 2nd phase, takes a few weeks, collagen fibers forms scar
tissue, and creation of tiny new blood vessels
 3rd phase takes months or years, scar tissue matures,
results to for stronger scars.
m ^oss of the ability to sweat
 Difficulty in hot and humid conditions.
m Dryness of skin due to loss of sebaceous glands.
m Color changes
m changes in strength of skin
 Healed scars are about 20% weaker than the skin they
replace
m Change in sensation
m !ain
 èeeling of skin tightness, numbness or tingling or burning
sensation
m Run cool water on burned area for 5-0 mins,
cover with cool compress
m Don¶t apply oil, butter, or ice on burn area
m Do not break blisters
m Do not remove clothing stuck to skin
m Elevate burned area
m C!R
m Dermabrasion
 Ôcraping away the outmost layer of the skin with a rough
wire brush or a burr containing diamond particles
attached to a motorized handle
m Dermaplaning
 Use dermatone, used for skimming off layers of skin that
are irregular
m Exercises
m Bandaging
m !u
m !ain
m èluid and electrolyte imbalance
m èluid volume deficit
m Ôupply blood and oxygen to the tissues
m 2 main actions:
 Ôystole
˜ Contraction
˜ Ejection of blood
 Diastole
˜ Relaxation
˜ èilling of blood
m 3 physiological characteristics of cardiac
conduction cells
 Automaticity
˜ Ability to initiate electrical impulses
 Excitability
˜ Ability to respond to an electrical impulses
 Conductility
˜ Ability to transmit an electrical impulse from one cell to
another
m ÔA node (sinoatrial node)
 !rimary pacemaker of the heart
 Inherent firing rate of 60- 0 bpm
 ^ocated a the right atrium
 ë   

m AV node (atrioventricular node)
 Coordinates the incoming electrical impulse of ÔA node
 èacilitate a delay allowing ventricular filling
 Inherent firing rate of 0-60 bpm
m Bundle of His
m ^eft bundle branch
m Right bundle branch
m !urkinje fibers
 Ôite where myocardial cells are stimulated causing
ventricular contractions
 Inherent firing rate of 30-0 bpm
m Due to movement of ions (charge particles such
as Na, Ñ, Ca) across cell membrane
m Cardiac action potenctial
 Electrical changes recorded within a single cell
m !olarized cardiac muscle cells
 An electrical difference exists in and outside the cell.
m Depolarization
 Electrical activation of the cell, internal charge to positive
one.
m Electromechanical coupling
 If muscle cells depolarized acts as a stimulus to its
neighboring cells causing contract
m Repolarization
 Return of cells to its resting state
 Relazation of myocardial muscle
m Refractory period
 Ôustained contraction
 During which the muscle cannot be restimulated
 !rotects the heart from sustaining contraction (tetany)
m uhe volume of blood pumped by the ventricle of
the heart by each beat.
m !reload
 Degree of stretch of the cardiac muscle fibers at the end
of the diastole (relax)
 Greater length, greater degree of shortening
m Afterload
 Amount of resistance of ejection of blood from the
ventricle
m Contractivity
 èorce generated by the contraction of the myocardium
 Decreased by hypoxemia, acidosis, medications
m Ejection fraction
 !ercentage of the end diastolic volume that is ejected
with each stroke.
m Disorders in the conduction
m May be initially evident by hemodynamic effect
they cause like, change in conduction,pumping
action of the heart and decreasing B!
m uhey are named according to site of origin of
impulse and the mechanism of formation
conduction involved.
 Etc. Impulse that originate in the ÔA that has a slow rate
is called    
m Normal electrical impulse values at a rate between
60-00 bpm
m Electrical impulses that travels thru the heart can
be seen in an 

m  creates an immaginary line called

m   represents the function of the
heart conduction system.
m
 or are measured on ventrical
axis
m uand are measured on the horrizontal
axis.
m !  are waves move toward the
top of the paper.
m î moves towar the bottom of
the paper.
m !-wave
 Electrical impulse of the ÔA spreading thru the atria
 Represtence atrial muscle depolarization.
 Normally 2.5mm or less in height
m ·RÔ complex
 Represents ventricular muscle depolarization
 Not all ·RÔ can have all 3 wave forms
 Is normally less than 0.2mm
m · wave
 st negative deflection normally less than 0.0 sec and
less than 25% of the R wave amplitude.
m R wave
 st positive deflection afer ! wave
m Ô wave
 st negative deflection after R wave
m When a wave is less than 5 mm in height small
letters are used,but if taller than 5 mm capital
letters.
m u wave
 Represents venticular muscle repolarization
 èollows afte the ·RÔ complex
m U wave
 Represents repolarization of !urkinje fibers seen in
patient with hypokalemia, hypertension and heart
disease.
 Ômaller than the ! wave
m Ôu segment
 Early ventricular repolarization
 ^ast from the end of the ·RÔ Complex to the begining of
the u wave
 Its end is difficult to identify because it merges into the u
wave.
 Is normal isoelectic
 It is analyzed to identify whether it is above or below the
isoelectic line which may be among other sign and
symptoms of cardiac ischemia
m ·u interval
 uotal time of ventricular depolarization and repolarization
 Measured from the begining of the ·RÔ complex to end
of u wave.
 Is usually 0.32-0.0 mm
 If it is prolonged patient may be risk for a lethal
ventricular dysrhythmia
m u! interval
 End to the u wave to begining of the next ! wave
 An isoelectric period
m !! interval
 ! wave to the next ! wave
 Atrial rhythmand atrial rate
m RR interval
 ·RÔ complex to the next ·RÔ complex
 Used to determine ventricular rate and rhythm
m Ôinus tachycardia
 Wave of impulse is transmitted through the normal
conduction pathways sinus stimulation is simply greater
than normal 00 bpm
 Rate: 30 bpm
 Rhythm: R-R interval are regular
 ! wave: present for each ·RÔ complex, normal
configuration, identical
 ·RÔ complex: normal in appearance, one follows each !
wave
m Ôinus bradycardia
 Vagal tone are stimulated sinus node is to slow
 MI, scarring of the ÔA node
 ^ess than normal (less than 60bpm)
 Rate: 55
 Rhythm: R-R is regular
 !-wave present for each ·RÔ complex, normal
configuration and each ! wave is identical
 Atropine sulfate 0.5mg IV push
m !remature atrial contraction
 A precursor of more serious dysrhythmias in the diseased
heart.
 Rate: may be slow or fast
 Rhythm: will be irregular
 ! wave: will be present for each normal ·RÔ complex;
the ! wave of the premature contraction will b distorted in
shape.
 !-R interval: may be normal or may be shortened
 ·RÔ complex: within normal limits
 Requires no treatment but should be monitored
m !aroxysmal Atrial uachycardia
m Causes include syndrome of accelerated
pathways (Wolff-!arkinson-White Ôyndrome),
Ôyndrome of mitral valve prolapse, Ischemic
coronary artery disease, excessive use of alcohol,
cigarettes, caffaine, drugs
m uhe rate is often so rapid that the ! waves are not
obivious.
m Rate: between 50 and 250 bpm
m Rhythm: regular
m ureatment is directed first to slowing the rate and
reverting the dysrhythmia to a normal sinus rhythm
m Reducing the rate may be accomplished by having the
patient preform valsalvas maneuver.
m Adenosine(Adenocard) is the drug of choice for !Au
associated with hypotension, chest pain and shortness
of breath
 Ôlows conduction time through the A-V node
m Beta-adrenergic blockers, esmolol (Brevibloc)
m Calcium channel blockers, Calan and Verapamil
m Artial èlutter
m Due to atrial stretching or enlargement in MI, and
CHè
m AV node setup a theraputic block, which disallows
some impulse transmission
m Rate: between 250-00bpm
m Rhythm: regular or irregular
m ! wave: not present; instead it is replaced by a
sawtoothed pattern that is produced by the rapid
firing of the artia. uhese waves are also referred to
as ³è waves
m Calcium channel blocker diltiazem (Cardizem)
may be used to slow AV nodal conduction
m Digitalis and quinidine
 Has anti-arrhythmic effects
m Beta-adrenergic blockers
m Cardioversion, dose of small amount of electrical
current
m Atrial èibrillation
m Aging process, MI, valvular disease
m Rate: atrialfibrillation is usually immeasurable
because fibrillatory waves replace ! waves,
ventricular rate may vary from bradycardia to
tachycardia.
m Rhythm: classically described as an irregular
irregularity
m ! wave: replaced with little ³f waves
m ureated with digitalis preparations
m Cardioversion
m Beta- adrenergic blockers
m Adenosine (adenocard)
m is a progressive disorder in which damage to the
heart causes weakening of the cardiovascular
system.
m Manifest with fluid congestion or inadequate blood
flow to tissues
m Heart failure is a cumulative consequence of all
insults to the heart over someone's life.
m It can affect the lungs, neuroendocrine system,
kidneys and other organs
m èluid congestion
 If there is insuffiecient pumping of the heart or the
circulation, the body will compensate for it, by use of
hormones or nerve signals to increase the blood volume
 Blood and fluids backed up behind the the heart resulting
to excessive water entering the lungs
 Edema and dyspnea will be present
m Reduced blood flow to the body
 Difficulty of exercising
 èatigue
 Dizziness due to decreased blood pressure
m Right vs. ^eft Ôided Heart èailure
 @
 - uhe inability of the right side of the
heart to adequately pump venous blood into the
pulmonary circulation. uhis causes a back-up of fluid in
the body, resulting in swelling and edema.
 ^ - uhe inability of the left side of the
heart to pump into the systemic circulation. Back-up
behind the left ventricle causes accumulation of fluid in
the lungs.
m As a result of those failures, symptoms can be due to:
m   - uhe inability of the heart to
pump blood at a sufficient rate to meet the oxygen
demands of the body at rest or at exercise.
m O  - uhe ability of the heart to
pump blood at a sufficient rate ON^ when heart filling
pressures are abnormally high.
m    - èluid in the lungs or body,
resulting from inadequate pumping from the heart and
high heart filling and venous pressures.
m Chest x-ray
m 2D echo
m ECG
m uracer studies
 Radioactive tracers through IV
m ureadmill test
m Angiography
m re-establish perfussion and oxygenation
m Vasodilators (nitroglycerine), diuretics
(furosemide)
m ACE inhibitors (enalapril, captopril)
m Beta blockers
m Excersises can be encouraged as tolerated
m Cardiac transplantation