B Io Crisis

BI OLOG IC CRI SI S
Dr. Anthony Toledo MD,RN

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SHOCK DM/DKA
ARRHYTHMIAS KIDNEY FAILURE (ERDS)
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Wh at is Sh ock ?
 A condition in which systemic BP is adequate to

deliver oxygen and nutrients to support vital
organs and cellular functions.
 Maintenance of tissue perfusion depends on

adequate cardiac pump, effective vasculature or
circulating system and sufficient blood volume.
 Widespread serious reduction of tissue

perfusion ( lack of O2 )
Cla ss ifica tion of s hock
A. HY PO VO LEMI C SHO CK
 Loss of circulating volume due to excessive

blood loss, loss of body fluids and third spacing
of fluids.
 Most common type of shock.
 Characterized by decreased intravascular

volume of 15-25%.
HYP OVO LEM IC SH OCK
Predi spos in g fa ct or s:
External:FluidLoss
Internal:FluidShift
 trauma a. hemorrhage
 surgery b. burns
 vomiting c. ascite
 diarrhea d. peritonitis
 diuresis e. dehydration
 diabetes insipidus
Med ica l M an agemen t
GOALS:
 restore intravascular volume
 redistribute fluid volume
 correct the underlying cause
Fl ui d and Bl ood re plac ement :

• Lactated Ringer’s solution, colloid, and 0.9% NaCl (normal saline) to restore intravascular
volume.
• Blood replacement for extensive and rapid blood loss; auto-transfusion methods may be
considered for closed cavity hemorrhage.
Red ist ri but ion of Flui ds

• Patients is positioned in trendelenburg to assist in fluid redistribution.
•Military antishock trousers (MAST) are used in extreme emergency situations when bleeding
cannot be controlled
Ph arma colog ic Ex am
 Desmopressin
 Insulin
 Anti-emetic
 Anti-diarreal
Nu rs in g M anagemen t
 Closely monitor px at risk for fluid deficits(younger than 1y/o or
65 years of age)
 Assist with fluid replacement
 Ensure safe administration of of prescribe fluids and

medications, and document effects
 Monitors and report signs of complications and effect of

treatment.
 Monitor for cardiovascular overload and pulmonary edema:

hemodynamic pressure, VS, ABG, and fluid IO.
 Reduce fear and anxiety about the need for oxygen mask by
giving px explanations and frequent reasurance
Ca rdiog en ic Sh oc k
Ca rdiog en ic Sh oc k
 The ability of the heart to pump blood is impaired

that causes a decrease in cardiac output.
 Causes of cardiogenic shock are either coronary or

noncoronary
 Coronary cardiogenic shock is more common and

seen most often in px with myocardial infarction.
 Noncoronary causes include tension pneumothorax,

sever metabolic problem, cardiac tamponade,
cardiomyopathy, valvular damage and dysrhythmias.
Pa th oph ysi o o f C ar di ogen ic
Shock
Clin ica l M anif estation :
 Dysrhythmias are common and result from a decrease in

oxygen to the myocardium.
 Angina pain
 Hemodynamic instability
 Classic sign like low blood pressure, rapid and weak pulse.
 Cerebral hypoxia and manifested by confusion and agitation.
 Deceased urinary output and cold clammy skin.

 correction of underlying cause
 initiation of first line treatment
Ø supplemental oxygen
Ø controlling chest pain
Ø selected fluids support
Ø vasoactive medications
Ø controlling heart rate
Ø mechanical cardiac support
e.g intra-aortic balloon counterpulsation, ventricular
assist sysytem.
 Coronary cardiogenic shock is treated with thrombolytic theraphy,

angioplasty, or CABG
 Noncoronary cardiogenic shock is treated with cardiac valve
replacement or correction of dysrhythmias.
Ph arma colog ic
 Dobutamine
 Dopamine
 Anti-arrythemic meds
 Nitroglycerine
 Vasoactive meds
 Preventing cardiogenic shock
 Administering meds and IV fluids
 Maintaining mechanical devices
 Enhancing safety and comfort

Distri buti ve Sho ck / V aso genic
Shock ( Ci rcu latory Shock )
 Result from profound vasodilation
 Three classification of distributive shock:

Septic shock, Anaphylactic shock and
Neurologic shock
Sep tic Sh ock
Sep tic Sh ock
 The most common type of distributive shock,

is caused by widespread infection.
 Gram-negative bacteria are the most common

pathogens.
 Gram-positive bacteria and viruses and fungi,

can also cause septic shock
Ris k f act or s:
 Immunosuppression
 Extremes of age ( younger than 1y/l and older
than 65y/o)
 Alcoholism
 Extensive trauma of burns
 Malnutrition
 Diabetes
 Malignancy
 Chronic illness
 Invasive procedures
Pathop hysiolog y
 Microorganism invasion causes immune response that

activates biochemical mediators associated with
inflammatory response and produces a variety of
effects leading to shock.
 There is an increase in the capillary permeability, with

fluid loss from the capillaries and vasodilatation,
result in inadequate perfusion of oxygen and
nutrients to the tissue and cell.
Clin ica l M anifes tatio n
Fir st ph as e: Hyperd ynami c o r Prog res sive phas e
 High cardiac output with vasodilation
 Hyperthermia (febrile) with warm, flushed skin, bounding pulses
 Heart and respiratory rate elevated
 Blood pressure may remain within normal limits, or subtle changes in mental
status.
 Decreased urinary output or normal
 Gastrointestinal status compromised (eg, decreased bowel sounds, n/v or
diarrhea)
Late ph as e: Hypody nami c or Ir re vers ib le p hase

 Low cardiac output with vasoconstriction
 Decreased blood pressure
 Skin cool and pale
 Temperature normal or below normal
 Rapid respiratory and heart rate
 Anuria and multiple organ dysfunction
Sep tic Sh ock
 Urine, blood, sputum, and wound drainage specimens

are collected to identify and eliminate the causes of
infection.
 Begins immediately a broad-spectrum antibiotic

therapy
 Fluid replacement and aggressive nutritional

supplement (high protein) is provided. Enteral
feedings are preferred.
 Identify px at risk for sepsis and septic shock
 Monitor for sign of infection at intravenous lines, arterial and venous

puncture sites, surgical incisions, trauma wounds, urinary catheters and
pressure ulcer
 Reduce px temp. when ordered for temp above 104.8F (40.8C) monitor
closely for shivering
 Administered prescribed intravenous fluids and medications
 Monitor and report blood levels (antibiotics, BUN, creatinine, WBC ) and
hemodynamic status, fluid IO and nutritional status.
 Monitor daily wts. And serum albumin levels to determine daily protein
requirements
NE UR OLOG IC SHO CK / S PI NAL
SHOC K
 There is loss of vasomotor tone that

includes arteriolar and venous
dilatation .
 Spinal cord injury
 Spinal anesthesia
 Depressant meds
 Hypoglycemia
 Restoring sympathetic tone

 Elevate the head of the bed 30 degrees ( in spinal / epidural anesthesia )
 Immobilize the patient ( in spinal cord injury )
 Elastic compression stockings
 Feet elevation
 Heparin / low molecular weight heparin
 Pneumatic compression of the legs
 Passive ROM
An aphylactic S hock
An aphylactic S hock
 An antigen-antibody reaction brought about by

severe allergenic reaction provokes mast cell to
release chemical mediators like histamine and
bradykinin widespread vasodilatation and capillary
permeability.
 Drug sensitivity
 Transfusion reaction
 Bee sting allergy
 Latex sensitivity
 Rremoval of causative agent
 Restore vascular tone ( epinephrine )
 Antihistamines and bronchodilators

 Assess for previous hypersensitivity reactions
 Prevention of future exposure to antigens
 Identification of new antigens
 Patient education
Sta ges of Sh ock
INITI AL STAG E / C OMP EN SATED / NONPR OGRESS IVE

SH OCK
 BP is maintained within normal limits due to the effect

of normally functioning regulatory mechanisms
 Blood loss less than 10%

Sig ns an d Symp tom s
 Apprehension and restlessness ( 1st sign of

shock )
 Increase heart rate
 Cool, pain skin
 Metabolic acidosis
 Fatigue
 Tachypnea
 Mental status change
 Identify the cause of shock

 Correction of shock
 Support of the regulatory
mechanisms
 Monitoring tissue perfusion

Ø LOC
Ø V/S
Ø Urine output
Ø Skin
Ø Laboratory values
 Reducing anxiety
 Promoting safety
Pr ogr essi ve Sta ge /
Dec om pen sa te d
 Exhaustion of the compensatory mechanism
 Myocardial depression
 Increased capillary permeability

Sign s an d Sy mptoms
A. Re spi ra tory ef fect s
Ø hypoxemia and hypercarbia
Ø intense inflammatory response
Ø decreased surfactant production
Ø acute respiratory distress syndrome ( acute lung injury, shock
lungs, non cardiogenic pulmonary edema )
B. Ca rd iova scu la r ef fect s

Ø dyshrythmias
Ø myocardial infraction
Ø cardiac depression
C. Neu rologi c ef fec ts

Ø decreased cerebral perfusion
Ø mental status change
Ø behavioral change
Ø papillary dilation
Sign s an d Sy mptoms
D. Renal effects
Ø MAP<80mmHg
Ø Acute renal failure
E. Hepatic effects
Ø Decreased blood flow
Ø Less ability to perform hepatic functions
F. gastrointestinal effects
Ø Decreased blood flow
Ø PUD
Ø Bloody diarrhea
Ø Sepsis
 Depends on the type of shock
 Depends of the decompensation of the

organ systems
Irr ev ersib le St age
 Sever organ damage
 Can no longer respond to treatment
 Survival is less likely

 Same with progressive stage

 Same with progressive shock
 Moral support to the family
 Ethical issue ( living will )

As ses smen ts
A. Ea rl y stage s
Ø Restlessness, confusion
Ø Increase RR and PR, respiratory alkalosis
Ø Diaphoresis, cool clammy skin/warm, flushed skin in septic shock
Ø Normal to decreased urine output, thirst, dry mucous membrane
Ø Hypokalemia
B. La te sta ges
Ø Shallow respiration, decreased BP, increased PR, hypothermia
Ø Oliguria, Anuria
Ø Hyperkalemia
Ø Metabolic acidosis
Ø Edema
Ø Cool clammy skin- hypovolemic, cardiogenic and septic shock
Ø Lethargy, dilated pupils
Ø Decreased bowel sounds
Ø Cyanosis
Ø DIC
Interv en tion s
A. Promoti ng flu id s balance
Ø Blood transfusions
Ø IV fluids
B. A ssistin g wit h car diac support

Ø Intraaortic balloon pump ( IABP)
Ø Medical anti-shock trousers
Ø Modified trendelenburg position
C. As sis ti ng res pira to ry suppo rt

Ø O2 therapy
Ø Mechanical ventilator
Ø Deep breathing, coughing excercises
Ø Suction as necessary
In terven tion s
D. Ass istin g wi th renal support

Ø Monitor I and O, BUN and creatinine
Ø Diuretics
E. Ass is tin g with GI sup port

Ø NGT
Ø H2 blockers and antacids
F. Promotin g sa fety
Ø Soft restraints as needed
Ø Practice strict asepsis
Ø Prevent complications of immobility
Ø Protect from chills
Drug Th er apy
 Vas oco nst ri ct ors:
Norepi ne phr ine / epi nep hri ne, do pa min e, dobu tam
 Vaso dila tors:
Nitr ate s lik e nitr ogly cer ine an d Iso so rb ide
 Na+ bicarbonate to reverse acidosis
 Antibiotics to control sepsis
 Heparin to treat DIC
 Steroids to reduce inflammation
 H2 antihistamines, Ranitidine, cimetidine
 Glucose 50% or glucagons to increased blood sugar
 Narcotics for pain
 Antidysrrhythamic drugs
End of the slides
Arrh yth mia s
Card ia c Arr hythmia s
 It is an abnormal electrical conduction

or automaticity causing changes in
the heart rate and rhythm.
 Congenital
 Myocardial Ischemia
 MI
 Organic heart disease
 Drug effect and toxicity
 Conductive tissue degeneration
 Electrolyte imbalance
 Acid-base imbalance
 Cellular hypoxia
Pathop hysiolog y
 Result in the disturbance in the excitability,

automaticity, or conductivity
 Heart rate and rhythm are altered, reducing

cardiac output
As ses smen t
 Asymptomatic  Syncope
 Palpitation  LOC
 Chest pain  Diaphoresis
 Dizziness  Pallor
 Weakness, fatigue  N/V
 Feeling of impending doom  Cold, clammy skin
 Irregular heart rhythm  Life-threatening:
 Bradycardia or tachycardia pulselessness, (-)
respiration, no palpable
 hypotension
blood pressure
Di agn osi s
 ECG- change in heart rate, rhythm
 Blood chemistry : electrolyte

imbalance
Nor ma l Sin us R hyth m
Nor ma l Sin us R hyth m
Occurs when the electrical impulse starts at the

regular rate and rhythm n the sinus node and travels at
through the normal conduction pathway
Ch aract erist ics :
 Vent ri cula r a nd a tri al ra te : 60 to 100 in

adult
 Vent ri cula r a nd a tri al rhyt hm : Regular
 QR S d ura tion: Usually normal, but may be
regularly abnormal
 P w ave : Normal and consistent shape; always
in front of QRS
 PR int erva l: Consistent interval between 0.12
and 0.20 seconds
 P: QRS ratio 1:1
Typ es o f S inus n ode
Dy srh ythm ias
A. Sinus Bra dyc ar dia
occurs when the sinus node creates an impulse
at a slower rate than normal.
 Vent ri cula r a nd atr ia l r ate : Less than 60 in
adult
 Vent ri cula r a nd atr ia l r hyt hm : Regular
 QR S d ura tion: Usually normal but may be
regularly abnormal
 P w ave : Normal and consistent
interval between 0.12 and
0.20 seconds
Sin us B rad yca rdia
Managemen t
 The urgency of treatment depend is on the effect of the

slow rate on maintenance of Cardiac output
 Atropines, 0.5 to 1.0 mg given IV push block vagal

stimulation to the SA Node & therefore accelerate heart
rate.
 If the bradycardia persists a pacemaker may be

required.
Types of Sinus Node
Dysrhythmias
B. Sinus Tac hyc ar dia

 Occur when the sinus node create
an impulse at a faster than normal
rate. It may be caused by acute
blood loss, anemia, shock,
hypervolemia, hypovolemia CHF,
pain, hypermetabolic states, fever,
anxiety or sympathomimetic
medication.
Characteristics:
 Vent ri cular and atri al ra te: Greater
than 100 in the adult
 Vent ic ula r and atr ia l rhyt hm : Regular
 QRS dura tio n: Usually normal, but may
be regularly abnormal
 P wave : Normal and consistent shape,
always in front of the QES, but may be
buried in the preceding T wave.
Sinus Tachycardia
As the heart rate increases, the diastolic falling time decreases, result in
reduced cardiac output and subsequent symptoms of syncope and low
blood pressure. If the heart cannot compensate for the decreased
ventricular falling the px may develop acute pulmonary edema
Ma nag eme nt
 It is usually directed at abolishing its

causes.
 Calcium channel blockers and Beta-blockers

may be used to reduce the heart rate
quickly.
Ty pes of Sin us n od e
Dysrh yth mia s
C. Si nus Ar rhyt hmi as
Occur when the sinus node create an

impulse at an irregularly rhythm; the rate usually
increase with inspiration and decrease with
expiration. Non respiratory cause includes heart
disease and valvular disease, but these are rarely
seen.
Ch aract eris tics :
 Ven tricu lar an d at ria l rat e : 60 to 100 in the adult

 Ven tricu lar an d at ria l rhyt hm : Irregular
 QRS du rat io n: Usually normal, but may be regularly
abnormal
 P wa ve : Normal and consistent shape, always in front of
the QRS.
 PR i nter va l : Consistent interval between 0.12 and 0.20
second
 P: QRS ratio: 1:1
*Sinus Arrhythmia does not cause any significant hemodynamic

effect and usually is not treated.
Atria l D ysrhythmia s
A. Pr emat ure At ria l Com plex

 Premature Atrial Complex Is a single ECG complex that
occur when an electrical impulse start in the atrium
before the next normal impulse of the sinus node.
 The PAC may be caused by caffeine, alcohol, nicotine,

stretched atrial myocardium, anxiety hypokalemia (low
potassium level), hyper metabolic states or atrial
ischemia, injury or infarction.
 Ven tricu lar an d at ria l rat e : Depend on the underlying
rhythm
 Ven tricu lar an d at ria l rhyt hm : Irregular
 QRS du rat io n: The QRS that follows the early P wave is
usually normal, but it may be abnormal.
 P wa ve : An early and different P wave may be seen or
may be hidden in the T wave;
 Other P wave in the strip is consistent.
 PR i nter va l: The early P wave has a shorter than normal
PR interval, but still between
 0.12 And 0.20 seconds
 P : QRS ratio: Usually 1:1
Managemen t
 If PACs are in frequent, no treatment is necessary. If

they are frequent (more tan 6 per minute) this may
herald a worsening diseases state or the onset of
more serious dysrhythmias, such as atrial fibrillation.
Treatment is directed toward the cause.
 PAC’s should be monitored for increasing frequency

At ria l F lu tter
Atria l Dysrhythmia s
B. At ri al Fl utt er
 Occur in the atrium and creates impulse at an atrial
rate between 250 and 400 time per minute.
 Because the atrial rate is faster than the AV node can

conduct, not all atrial impulse are conducted into the
ventricle causing a therapeutic block at the AV node.
At ri al Flu tter
 Vent ri cula r a nd atr ia l r ate: Atrial range

between 250 and 400 ventricular rates usually
 Range between 75 and 150
 Vent ri cula r a nd atr ia l r hyt hm : Usually
Regular
 P w ave : Saw –toothed shape. These waves
referred to as F wave
 PR i nt erva l; Multiple F waves may make it
difficult to determine the PR interval.
 P : QRS ratio: 2:1, 3:1, or 4:1
Sign and Sy mptoms
 Chest pain
 Shortness of breath
 Low blood pressure.
Ma nag emen t
 The urgency of treatment depend on the ventricular response rate&

resultant symptoms
 A Calcium channel blocker such as Diltiazem (cardizem) may be use to

slow AV Nodal conduction used with caution in the patient with CHF,
hypotension
 Digitalis & Quinidine preparation may be used.
 A beta –adrenergic block drug such as Esmolol may be used.

 If drug therapy is un successful, trial flutter will often respond to
cardivertion.

Small doses of electrical current are often successful
At ria l Fi brilla tion
Atria l Dysrhythmia s
C. At ri al Fibr ill at ion

 May occur for a very short time (paroxysmal) or it may be chronic
 It is the most common dysrhythmias that cause patients seek medical

attention
 The shorter time in diastole reduce the time available for coronary
artery perfusion, there by increasing the risk for myocardial ischemia.
 The erratic atrial contraction promotes the formation of a thrombus

within the atria increasing the risk of stroke (brain attack).
 Vent ri cula r a nd atr ia l r ate: Atrial rate is 300
and 600 in untreated atrial fibrilation
 Vent ri cula r a nd atr ia l r hyt hm : Highly irregular
 QR S s ha pe a nd d ura tion: usually normal but
may be abnormal
 P w ave : No discernible P waves; irregular
undulating waves are seen and are referred to as
fibrillatory or waves.
 PR i nt erva l: Cannot be measured
 P : QRS ratio: many:1
Managemen t
 Cardiovertion may be indicated for atrial fibrillation that has been present for less
than 48 hours, a condition termed acute onset of atrial fibrillation
 Acute onset, the medication quinidine,
 Ibutilide,flecanide, dofetilide, profafenon, procanamide, dysopyramide or

amiodirone may be given to achieve convertion to sinus rhythm
 Intravenouse adenosine (adenocard,adenescan) has also been use for convertion,

as well as to assist in the diagnosis.
 Calcium channel blocker and beta blocker are effective in controlling the
ventricular rate in atrial fibrillation
 Use Digoxin is recommended to control the ventricular rate those patient with
poor cardiac function
 Aspirin may be substituted for warfarin.

At ria l Fi brilla tion
Juncti onal D ys rh ythmias
A. Pr emat ure Junc ti on Co mpl ex
 Is an impulse that starts in the AV nodal before the next normal sinus
impulse reaches the AV node Premature junction complex are less common
than PAC’s
 The criteria for premature junction complex are the same as for PACs except
for the Pwave and the PR interval. The Pwave may be absent QRS, or may
occur before the QRS but with a PR interval of less than 0.12 second
 Treatment for frequency premature junction complexes is the same as for

frequent PACs.
Premat ure J unct ion
B. J un ct io nal Rhy thm
Jucntional or idionodal rhythm occur when the AV

node, instead of the sinus node, become the
pacemaker of the heart.
Ch ara ct eris tics :
 Vent ricul ar a nd a tri al ra te: 40 to 60
 Vent ricul ar r hyth m : Regular
 QR S dura tion: Usually normal but may be
abnormal
 P w ave : May be absent, after the QRS complex,
or before the QRS; may be invented, especially in
lead II
 PR int erva l: If P wave is in front of the QRS, PR
interval is less than 0.12 second
 P: QRS ratio1:1 or 1:1
C. At ri ove nti cul ar Noda l Reentr y

Tachyc ardi a
 Occurs when an impulse is conducted to an area in the AV node
that causes the impulse to be rerouted back into the same area over
and over again at a very fast rate.
 It has an abrupt onset and an abrupt cessation with a QRS of normal

duration had been called paroxysmal atrial tachycardia (PAT)
 Vent ricul ar a nd a tri al ra te: atrial rate 150-
250; vent rate: 75-250
 Vent ricul ar a nd a tri al rhyt hm : Regular;
sudden onset and termination of the tachycardia
 QR S dura tion: Usually normal but may be
abnormal
 P w ave : usually very difficult to discern
 PR int erva l: If P wave is in front of the QRS, PR
interval is less than 0.12 second
 P: QRS ratio1:1 or 2:1
Ven tri cu lar
Dysrhyt hmia s
A. Pr emat ure Ven tricu lar Co mp lex
 Caused by acute MI other form of heart disease, pulmonary disease,

electrolyte disturbance, metabolic instability and drug abuse
 The wave of impulse originates from an ectopic Focus (Foci) within the
ventricles at rate faster than the next normally occurring beat.
 Because the normal conduction pathway is by passed configuration of

the PVC is wider than normal and is distorted in appearance.
 PVC’s may occur in regular sequence with normal rhythm.

Prem ature Ve ntricu la r
Com plex
 Vent ricul ar a nd a tri al ra te: Depend on the
underlying rhythm.
 Vent ricul ar a nd a tri al rhyt hm: Irregular
 QR S dura tion: 0.12 second or longer shape is
bizarre and abnormal
 P w ave : none
 PP int erval : If the P wave is in front of the QRS,
the PR interval is less than 0.12 second
 P : QRS ratio 0:1, 1:1
Managemen t
 The standard treatment is Lidocaine hydrochloride (Xylocaine) by

IV push
 Be alert to the development of confusion, slurring of speech and

diminished mentation because lidocaine toxicity affects the CNS.
 If ventricular premature beats occur in conjunction with

bradysrhythmias, atropine may be chosen to accelerate the heart
rate and eliminate the need for etopic beat.
 Atropine should be used with caution in acute MI. the injured

myocardium may not be able to tolerate the accelerated rate.
Ven tri cu lar
Dysrhyt hmia s
B. Ven tricu lar Ta chy car dia
 Ventricular tachycardia (VT) is designed as three or

more PVCs in a row, occurring at a rate exceeding 100
beat per minute.
 The causes are similar to those for PVC
 VT is an emergency because the patient is usually

unresponsive and pulse less
 Vent ri cular and atri al rate: 100to200

beat per minute
 Vent ri cular and atri al rhythm : Usually
Regular
 P wave : so atrial rate and rhythm may be
indeterminable.
 PR int erva l: Very Irregular
 P: QRS ratio: difficult to determine
Ven tri cu lar Ta ch yca rdia
Managemen t
 Cardiovertion may be the treatment of choice,

especially if the patient is unstable.
 VT in a patient who is unconscious and without a

pulse treated in the same manner as ventricular
fibrillation immediate defibrillation is the action of
choice.
Ven tri cu lar
Dysrhyt hmia s
C. Vent ri cular Fibri ll at io n
Is a rapid but disorganized ventricular rhythm that

cause of ventricular fibrillation are the same as
for VT, it may also result from untreated or
unsuccessfully treated VT. Other cause includes
electrical shock and Brugada Syndrome.
Ventricu la r Fib ril lat ion
 Ven tri cula r rat e: Great er than

300 per minute
 Ven tri cula r and a tri al rhyt m:
Extremely irregular
 QRS dura tio n Irregular
Managemen t
 Immediately fibrillation and activation of emergency service
 The importance of defibrillation is evident in one of the recent change

in basic life support.
 Placing a call for emergency assistant and calling for a defibrillator

takes precedence over initiating Cardio pulmonary resuscitation in
adult victim.
 Application of an automatic external defibrillator AED is included in

basic life support classes
 Administering Vaso active and anti arrhythmia medication alternating

with defibrillation are treatment used to try convert the rhythm to
normal sinus rhythm.
Ven tri cu lar
Dysrhyt hmia s
D. Idio vent ric ul ar Rhyt hm
 Is also called ventricular escape rhythm, occur when the impulse starts in
the conduction system below the AV node.
 Commonly cause the patient to lose consciousness and experience other

sign and symptoms of reduced cardiac out put . Intervention may include
identify the underlying cause, administering
 Intravenous atropine and vasopressor medication. Initiating emergency

transcutaneous pacing.
 Bed rest is prescribed so as not to increase the cardiac work load

 Ven tri cula r and a tri al ra te : Between

20and 40 if the rate exceeds 40, is known
(AIVR)
 Ven tri cula r and a tri al rhyt hm:
Regular
 QRS dura tio n : Bizarre, abnormal,
duration is 0.12 second or more.
Ven tri cu lar
Dysrhyt hmia s
E. Vent ric ular As ys tol e
 Commonly called flat line, ventricular a systole characterized

by QRS complexes, all though P wave may be apparent for a
short duration is two different leads. There is no heart beat,
no palpable pulse and no respiration.
 Assessment to identify the possible cause which may be

hypoxia, acidosis, severe electrolyte imbalance, drug overdose
or hypothermia.
Ven tricu la r As ystole
Managemen t
 CPR and emergency service as necessary to

keep the patient alive.
 Transcutaneuos pacing may be attempted. A

bolus of intravenous epinephrine should be ad
minister and repeated 3to5 minutes interval
End of the slides

HEAR T BL OCK
Conduct ion Ab norm alit ies
 The nurse first to identify is the underlying rhythm.(eg, sinus

rhythmia) then the PR interval is assessed for the possibility of an
AV block.
 AV block occur when the conduction of impulse through the AV

nodal are is decreased or stopped. These block can caused by
medication (eg,digitalis, calcium channel blockers, beta blocker).
 The Clinical sign and symptoms of a heart block vary with the
resulting ventricular rate and the severity of any underlying
disease processes.
 The treatment is based on the hemodynamic effect of the rhythm

Types of Con duct ion
Ab normalit ies
A. Fir st Degree Bloc k

Occur when all the atrial impulse
are conducted through the AV node into
the ventricle at a rate slower than normal
 Vent ri cular and atri al ra te: Depend

on the underlying rhythm.
 Vent ri cular and atri al rhythm : Depend
on the underlying rhythm.
 QRS dura tio n ; usually normal
 P wave : In front of QRS complex; shows
sinus rhythm, regular shape.
 P: QRS ratio1:1
Fir st D eg ree A V Block
Ab normalit ies
B.1 Seco nd Deg re e Atri oven tricu la r Block Type I
Second degree type I heart block occurs when all but one of the
atrial impulse are conducted. Through the AV node into the ventricles.
Each atrial impulse a take longer time for conduction than the one
before, until one impulse is fully blocked.
 Ven tricu lar an d at ria l rat e: Depend on the underlying

rhythm
 Ven tricu lar an d at ria l rhyt hm: The PP interval is
regular if the patient has an underlying normal sinus
rhythm; the RR interval characteristically reflect a pattern
of change .
 QRS du rat ion: Normal may be abnormal
 P wa ve : In front of the QRS complex; shape depend on
underlying rhythm
 PR i nter va l: PR interval become longer with each
succeeding ECG complex until there is a P wave not
followed by a QRS.
 P: QRS ratio 3; 2, 4:3, 5:4,
Second D egr ee A tri oventr ic ul ar
Bl oc k Typ e I
Ab norm alit ies
B.2 Sec ond Deg re e Atr iov entr icul ar Bl ock Typ e
II
Occur when only some of the atrial impulses

are conducted through the AV node into the ventricles
Se con d De gr ee Atriove nt ric ular
Block T ype II
 Ventricular and atrial rate: Depend on the

underlying rhythm
 Ventricular and atrial rhythm. The PP interval

is regular if the patient has an underlying
normal sinus rhythm.
Types o f Con duction
Ab normali ties
C. Thi rd Degree Atrio ve nt ri cular Blo ck
Occur when no atrial impulse is

conducted through the AV node into the
ventricle In the third degree heart block , two
impulse stimulate the heart :one stimulate the
ventricle ,represent by the QRS complex, and
one stimulate the atria .
Thi rd Degr ee Atri oventr icu lar
Bl ock
 Vent ri cula r a nd a tri al ra te: Depend on the

escape and underlying atrial rhythm.
 Vent ri cula r a nd a tri al rhyt hm :The PP
interval is regular and the RR interval is regular;
however the PP interval is not Equal to the RR
interval.
 QR S d ura tion : Depend on the escape of
rhythm
 P w ave : Depend on the underlying rhythm
 P: QRS ratio: More P wave than QRS complexes
Managemen t
 IF the patient is short of breath, complains of

chest pain or lightheadedness, or has low BP:
Intravenous bolus of Atropine is the initial
treatment of choice.
 If the patient does not respond to atropine or has

acute MI, trascutaneous pacing should be started.
 A permanent pacemaker may be necessary if the

block persist.
Nur si ng A ss ess ment
 Major assessment include all possible cause of the
dysrhythmia and the dysrhythmia’s effect on the heart’s
ability to pumped an adequate blood volume.
 When cardiac output is reduced, the amount of O2 reaching

the tissue and vital organ is diminished. This diminished
oxygenation produces the s/sx associated with dysrhythmia.
 A health history is obtained to identify any previous

occurrence of decreased cardiac output such as syncope
(fainting), lightheadedness , dizziness , fatigue, chest
discomfort and palpitation
 Coexisting condition that could be a possible cause of heart

block or dysrhythmia (heart disease, chronic obstructive
Nur si ng A ssess me nt
 All medications prescribed and over the counter
(supplements herbs and nutritional) may be reviewed.
 The nurse conducts physical assessment to the patient

with diminished cardiac output especially the level of LOC
. the nurse directs attention to the skin which may be
pale and cool. Sign of fluid retention, such as neck vein
distention and crackles and wheezes auscultated in the
lungs.
 The nurse auscultates for extra heart sounds ( especially

S3 and S4 ) and for heart murmur, measure blood
pressure indicates reduced cardiac output.
Nu rs in g D ia gnos is
 Decreased cardiac output

 Anxiety related to fear of the unknown
 Deficient knowledge about the dysrhythmias and its related
treatment.
Collaborative Problems and Potential Complication

 May developed over time a heart failure
 Thromboembolic
Nu rs in g I nter ven tion
1. Mo ni torin g an d man ag in g the dy sr hyt hmia s
 Regularly evaluate the blood pressure, pulse rate and rhythm, rate and
depth of respiration and breath sounds to determine the hemodynamic
effects.
 Obtain a 12 lead ECG, continuously monitor the patient and analyze

rhythm of the strips to track dysrhythmias.
 Use an antiarrhythmias medications and the nurse assess and observe

for the beneficial and adverse effects of each medications ad
prescribed.
 Assist the patient in developing a plan to make a lifestyle change that

eliminates or reduced the risk factors.
Nu rsing In terv en tion
2. Mi nimi ze anxie ty
 Maintain a calm and reassuring attitude
 Emphasized with the patient to promote a sense of confidence in living

the disease.
 Goal is to maximize the client’s controls and to make the unknown less
threatening.
3. Pr omo ti ng Home and Commu ni ty Based Car e
 Explain the importance of maintaining therapeutic serum levels of the

medications so that the patients understand why medications should be
taken regularly each day.
Adju ncti ve M oda li ti es a nd
Man agemen t
 Pacema ker the rapy – is an electronic device

that provide electrical stimulation to the heart
muscles. Used when the patient has a slower
than normal impulse formation or conduction
disturbance causing symptoms.
 Permanent pacemaker- are used commonly
irreversible complete heart block.
 Temporary pacemaker- are used to support
patients until they improve or receive a permanent
pacemaker.
Pa cema ker D es ig n a nd
types
 Pacemaker consist of 2 components : an electronic pulse generator and
pacemaker electrodes, which are located on leads or wire. The
generator contains the circuitry and batteries that generate the rate
and strength of the electrical impulse delivered to the heart.
 The pacemaker electrodes convey the heart’s electrical activity through

a lead to the generator ; the generator’s electrical response to the
information received is then transmitted to the heart.
 Leads can be threaded through a major veins into the right ventricles
(endocardial leads) or they can be lightly sutured onto the outside the
heart and brought the chest wall during open heart surgery.
Pa cema ker D es ig n a nd
types
 Epicardial wires are always temporary and are removed by
a gentle tug within a few daysafter surgery.
 Endocardial leads may be temporarily placed with

catheters through the femoral, antecubical, brachial or
jugular veins, usually guided by fluoroscopy.
 The energy source for permanent generators are:

mercury-zinc batteries (which last 3 to 4 years), lithium
cell units (up to 10 years), nuclear powered source such
as plutonium (up to 20 years).
 Block AV block usually 3 bundle branch

block
 Symptomatic Bradycardia
 Arrhythmia during surgery
 Sick sinus syndrome
 Mo nito ri ng Pacema ke r fun ct io n- observe the
presence of the pacemaker spikes in the ECG,
monitor for the pacemaker malfunctions, weakness,
dizziness, fainting, hypotension, shortness of
breath, chest pain, ankle swelling.
 Pr ev en t in fecti ons- changes the dressing

regularly and inspects the insertion site for redness,
swelling, soreness or any unusual drainage and
increase the temperature should be noted.
 Cl ie nt t each in g ab out pace make r-

instruct the patient how to check pulse at home, inform to
report any changes in the heart rate, avoid contact sports,
carry ID, instruct to report sign of battery failure, wear loose
fitting clothes, remind that most electrical appliances can be
used without interference the functions of the pacemaker,
avoid MRI, transmitter tower and anti theft device, move away
from electrical appliances that cause disturbances and
emphasize regular follow up check up.
End of the slides

STROKE
St rok e
Disrup tion of cereb ral circul at ion that resul ts in mot or and sensor y de fici ts
Caus es:
 Cerebral arteriosclerosis
 Syphilis
 Trauma
 Hypertension
 Thrombosis
 Embolism
 Hemorrhage
 Vasospasm
Ty pes of S trok e
1. Ische mic St roke

 Larg e Artery Thr omb otic Strokes - are due to atherosclerotic
plaques in the large blood vessel of the brain. Thrombus formation and
occlusion at the site of the atherosclerosis result in ischemia and
infraction and occur in older patients.
 Sma ll Penetratin g Artery Thr omb otic Strokes - affect one

or more vessels are the most common type of ischemic stroke. Also
called lacunar strokes. Occur in young ones.
Ty pes of S trok e
 Ca rd iogen ic Emb oli c Stroke s-

are associated with cardiac dysrhythmias, usually atrial fibrillation.
Emboli originated from the heart and circulate to the cerebral
vasculature, most commonly in the left middle cerebral artery,
resulting in a stroke. Embolic strokes may be prevented by the use
of anticoagulant therapy in patients with atrial fibrillation.
 Cr ypt ogen ic St ro ke - which have no known cause and

other stroke from cause of cocaine used, coagulopathies, migraine
and spontaneous dissections of the carotid or vertebral arteries.
 Numbness or weakness of the face, arm or leg especially on one side of the
body.
 Confusion or change in mental status
 Trouble speaking or understanding speech
 Visual disturbance
 Difficulty walking, dizziness or loss of balance or coordination
 Sudden severe headache

Clinical Man ifesta ti on
Mot or l oss
 A stroke is a lesion of the upper motor neurons and result in
loss of voluntary control over motor movements. Upper motor
neuron decussate (cross) a disturbance of voluntary motor
control on one side of the body may reflect damage to the
upper motor neuron on the opposite side of the brain.
 Most common motor dysfunction is hemi pl eg ia ( paralysis of
one side of the body) due to the lesion of the opposite side of
the brain.
 He mip ar es is or weakness of one side of the body
 Fl acc id pa ral ysi s and loss or decrease of deep tendon
reflex.
Com munic ati on Lo ss
 Dysa rthi a ( difficulty in speaking), caused by paralysis of the

muscles responsible for producing speech.
 Dysp ha si a or apha si a (defective speech or loss of speech)

which can be ex pr es siv e aph asia , rece pt ive aphasia or globa l
(m ixe d) aphasia
 Ap ra xia ( inability to perform a previously learned action) as may be

seen when a patient picks up a fork and attempts to comb.
Percept ua l Di stur ba nce
 Perception is the ability to interpret sensation
 Visual perceptual dysfunction are due to disturbance of the primary sensory
pathways between the eye and visual cortex.
 Hemianopsia (loss of half of the visual fields) may be occur from the stroke and
may be temporary or permanent.
 Disturbance in visual spatial relation ( perceiving the relation of two or more
objects in spatial areas) frequently seen in patient with right hemispheric damage.
Se nsory Loss
 Sensory loss from stroke may take the form of slight

impairment of touch or may be more severe, with loss of
proprioception ( ability to perceive the position and motion of
the body parts) as well as difficulty in interpreting visual,
tactile and auditory stimuli.
Sensor y Loss
 Sensory loss from stroke may take the

form of slight impairment of touch or may
be more severe, with loss of
proprioception ( ability to perceive the
position and motion of the body parts) as
well as difficulty in interpreting visual,
tactile and auditory stimuli.
Cogni ti ve Im pairm ent
 Such dysfunction may be attention span,

difficulties in comprehension, forgetfulness and
lack of motivation, which cause these patients to
become frustrated in their rehabilitation
program.
 Impaired physical mobility related to hemiparesis.
Loss of balance and coordination, spasticity and brain
injury.
 Acute pain (painful shoulder) related to hemiplegia and
disuse
 Self care deficit ( hygiene, toileting, grooming and
feeding) related to stroke sequelae
 Disturbed sensory perception related to altered
sensory reception, transmission and integration.
 Impaired swallowing
 Incontinence related to flaccid bladder, detrusor
instability confusion or difficulty in communicating.
 Disturbed thought process related to brain damage, confusion or

inability to follow instruction.
 Impaired verbal communication related to brain damage
 Risk for impaired skin integrity related to hemiparesis/ hemiplegia or

decreased mobility.
 Interrupted family process related to catastrophic illness and care giving

burdens
 Sexual dysfunction related to neurologic deficit or fear of failure

Di ag nos ic Te st F in din gs
 LP: increase pressure, bloody CSF

 CT scan: intracranial bleeding, infarct, or shift
of midline structures.
 EEG : focal slowing in area of lesion
 MRI : intracranial bleeding, infarct, or shift of
midline structures
 Brai n sc an: decreased perfusion
 Digit al subtr acti on Ang iography:
occlusion or narrowing of vessel
 Platelet inhibiting medication decrease the incidence of cerebral
infraction in patients who have experience TIA from embolic or
thrombotic cause
 Thrombolytic agents are used to treat ischemic by dissolving the

blood clot that is blocking blood flow to the brain. Recombinant t-PA is
genetically engineered form t-PA thrombolytic substance made
naturally by the body. It works by binding to fibrin and converting
plasminogen to plasmin which stimulate fibrinolysis of the
atherosclerosis lesion.
 The dose of t-PA minimum dose is 0.9mg/kg, the maximum dose is 90

mg. The loading dose is 10% of the calculated dose and is
administering over 1min. the remaining dose is administered over 1 hr
via an infusion pump. Then flushed the line with 20 ml of normal saline
solution.
 Vital sign monitored q 15min for the first 2 hrs,q30 min for the next 6
hrs.
 Bleeding is the most common side effects of t-PA administration and

the patient should be closely monitored.
 Other treatment are anticoagulant administration for ischemic stroke

and careful maintenace of cerebral hemodynamics to maintain cerebral
perfusion. Elevation of the head of the bed to promote venous
drainage and to lower increased ICP.intubation with an endotracheal
tube to established a patent airway.
 Endarterectomy for prevention of ischemic stroke is the removal of an

atherosclerotic plaques orthrombus from the carotid artery to prevent
stroke in patients with occlusive disease of the ectracranial cerebral
arteries
1. Imp rovi ng mo bi li ty and pr even ting jo int
def ormi ties
 correct positioning is important to prevent contractures

 Prevent adduction of the affected shoulder while the patients is in bed, a
pillow is placed in the axilla when where is limited external rotation; this
keep the arm away from the chest.
 Positioning the finger so that they are flexed while the hand placed on
slight supination which it is most functional position.
 The patients position should be changed every 2 hrs. toplace a patient in a
lateral position position, a pillow is placed between the legs before the
patients is turned.
 A full range of motion 4 to 5 times a day to maintain joint mobility and
regain motor control, prevent contractures, prevent further deterioration of
the neurovascular system
 Preparing for ambulation, the patient is taught to maintain balance while
sitting and then learn to balance while standing in a gradual manner until
the patient can walk.
1 Prev ent ing Shoul der pa in

 To prevent shoulder pain, the nurse should never lift the patient
by the flaccid shoulder or pull on the affected arm shoulder. If the
arm is paralyzed, subluxation at the shoulder can occur from over
stretching the joint capsule and masculature by the force of gravity.
 Amitriptyline hydrochloride used because of its sedating effects.
 Some clinicians advocate the use of a properly worn sling when the
patients first becomes ambulatory to prevent upper extremity from
dangling without support.
 ROM is important in preventing painful shoulder

3. M an ag e D ysph agia
 ET is reduced the risk of aspiration while the patient is in

ET tube elevate the head of the bed at least 30 degree to
prevent aspiration, check the proper position of the ET tube
before feeding the patients, ensure the cuff of ET is inflated
and give the formula slowly.
 Intermittent catheterization is used with patient with

bladder distention. And increased high fiber diet and
adequate fluid intake with patient with constipation
STRO KE
ISCHEMIC STROKE
HEMORRHAGIC STROKE
Hemor rh agic St ro ke
 Primarily caused by an intracranial or subarachnoid
hemorrhage, bleeding into the brain tissue, the
ventricles, or subarachnoid space.
 Intracerebral hemorrhage from spontaneous rupture of

small vessels account approximately 80% of
hemorrhagic strokes and caused by uncontrolled
hypertension.
 Secondary intracerebral hemorhage is associated with

arteriovenous malformation, intracranial aneurysm, or
certain medications (anticoagulants and amphetamines)
Hemor rh agic St ro ke
Pathop hysiolog y
Intr acere bral h emorrh age
 Bleeding into the brain substance, common in patients with hypertension and
cerebral atherosclerosis that causes rupture of the vessel
 Brain tumor and the use of medicines( oral anticoagulants, amphetamines and
illicit drugs such as crack and cocoaine).
 Bleeding occur mostly in the cerebral lobes, basal ganglia, thalamus, brain
stem (mostly pons) and cerebellum
Intr acrani al (Cereb ral) An eury sm
 Dilation of cerebral artery wall causes of weakness in the arterial walls.
 An aneurysm due to atherosclerosis, vascular disease, head trauma or

advance aging.
Pathop hysiolog y
Art eri oven ous Ma lfo rmat ion
 Due to an abnormality in embryonal development that leads to a tangle

of arteries and viens in the brain without acapillary bed. A cause of
hemorrhagic in young peoples.
Sub ara ch no id Hemorrh ag e
 May occur as a result of an AVM, intracranial, aneurysm, trauma or

hypertension
 There is a leaking aneurysm in the area of the circle of Willis or a

congenital AVM of the brain.
S
T
R
O
K
E
Clin ica l man if es tati ons
 Sudden, unusually severe headache and often loss of
consciousness for a variable period.
 Pain and rigidity at the bask of the neck (nuchal rigidity)

and spine due to meningeal irritation.
 Visual disturbance: loss of vision, diplopia, and ptosis

occur when the aneurysm is adjacent to the oculomotor
nerve.
 Tinnitus, dizziness and hemiparesis may also occur.

Ass essmen t
 Altered level of consciousness
 Sluggish papillary reaction
 Motor and sensory dysfunction
 Cranial nerve deficit (EOM, facial droop, presence of ptosis)
 Speech difficulties and visual disturbance
 Headache and nuchal rigidity or other neurologic deficit

 Ineffective cerebral tissue perfusion related to bleeding
 Disturced sensory perception related to medically

imposed restrictions (aneurysm precautions)
 Anxiety related to illness and / or medically imposed

restrictions.
 Bed rest with sedation to prevent agitation and stress management of
vasospasm and surgical and medical treatment to prevent rebleeding
 Analgesic prescribed for head and neck pain
 Elastic compression stockings to prevent DVT.
 Adequate hydration must be ensured to reduced blood viscosity and

improve cerebral blood flow.
 IV administration of calcium channel blockers, nimodipine which delay

the ischemic deterioration.
 Mannitol is given to reduced ICP, it acts by pulling water out of the

brain tissue by osmosis as well as reducing total body water through
diuresis.
Opti mizing Cerebra l Tis sue Pe rfusion
 Monitor blood pressure , pulse , level of responsiveness,

papillary reaction and motor functions hourly.
 Respiration status is monitored becaused reduction of O2

in the areas of the brain with impaired autoregulation
increased chances of cerebral infraction.
Imp lement in g An eury sm preca ution
 CBR with quite, non stressfull environment
 HOB elevated 15 to 30 degree to promote venous drainage and decrease ICP.
 Avoid Valsalva maneuver, straining , forceful sneezing, pushing up to bed, acute flexion or
rotation of the head and neck.
 No enemas are permitted but stool softener and mild laxative is prescribed.
 Dim light is helpful because of photophobia
 Coffee , tea, unless decaffeinated is usually eliminated.
 Wear antiemboic stocking to prevent DVT
 Observed for the s/sx of deep vein thrombosis such as tenderness, swelling, warmth,
discoloration, positive Homan’s sign report any abnormal findings
End of the slides

BURNS
Bu rns
 Burns are caused by a transfer of energy from a source to the

body.
 Categorized as thermal, radiation or chemical burn.
 There is a disruption in the skin that leads to increased fluid loss,
infection, hypothermia, scarring, compromised immunity and
changes in function, appearance, and body image.
 Young children and older people are at high risk for burn injury
 Younger than 5 years and older than 40 y/o are at high risk for
death after burn trauma.
Four major goals relating to burn:

 Prevention
 Institution of life saving measure for the
severely burned person
 Prevention of disability and
disfigurement
 rehabilitation
Pathop hysiolog y
Caused by transfer of energy form a heat source
to the body
Thermal, radiation or chemical burn
Tissue destruction results from coagulation,

protein denaturation, or ionization of cellular contents.
Depth of the injury depends on the temperature of the burning agent and the
duration of contact with the agent
Disruption of the skin can lead

Skin and the mucosa of Deep tissue can be increased fluid loss, infection,
hypothermia scarring
the upper airways are the damaged by electrical
compromised immunity, and
sites of tissue destruction burns or through changes in function, appearance,
prolonged contact with a and body image.
heat source
Clas si fica tio ns of B ur n
Ac co rd ing to D epth o f Ti ssu e
Destr uc tio n
A. Superficial Partial-Thicknes Burn
(first degree burn)
 The epidermis and possibly a portion of the

dermis are injured
 The damaged skin may be painful and appear

red and dry, as in sunburn, or it may blister.
Firs t D egree Bu rn
Classi fica tio ns of Bur n
Ac co rdi ng to D epth o f Ti ssu e
Destr uc tio n
B. Deep Partial – Thickness
(second degree burn)
 The epidermis and upper to uper deeper portion of the dermis are
injured. eg, scald
 The wound is painful, appears red, and exudes fluid. Capillary
refill follows tissue blanching.
 Hair follicles remain intact.
 Deep partial-thickness burns take longer to heal and are more
likely to result in hypertrophic scars.
Secon d D egree Bu rn
Cl assi fica tio ns of Bur n
Ac co rdi ng to D epth o f Ti ssu e
Destr uc tio n
C. Full – Thickness Burn
(third degree burn)
 Burn from a flame or electric current

 The epidermis, entire dermis, and sometimes the underlying
tissue are injured
 Wound color ranges widely from white to red, brown, or black.
 The burned area is painless because nerve fibers are destroyed.
And the wound appears leathery; hair follicles and sweat glands
are destroyed
Th ir d D eg re e Bu rn
Exten t of Bod y S ur face
Ar ea In ju red
A. In ner zo ne
 known as the area of coagulation, where cellular
death occurs
 sustains the most damage.
B. Mi dd le zo ne
 has a compromised blood supply, inflammation, and
tissue injury.
C. Outer zo ne
 the zone of hyperemia which sustains the least
damage.
RU LE O F NI NE
An estimation of the TBSA involved in a burn is simplified

9 by using the rule of nines.
It is a quick way to calculate the extent of burns.
The system assigns percentage in multiples of nine to major
body surfaces.
9 18 18 9 PARKLAND FORMULA
Computation of fluids
Most commonly used in burned patient
1
Formula: TBSA x 4ml x kg body weight
18 18 1st 8hrs give 50% of the formula

2nd 8hrs give 25% of the formula
3rd 8hrs give 25% of the formula
Meth ods i n D eter mi nin g the
Extent of Su rfac e Ar ea Bu rned
 Ru le of Nine : an estimation of the total body surface
area (BSA) burned by dividing the body into multiples of
nine.
 Lund and Browd er Me th od : a more precise method

of estimating the extent of the burn; the percentage of
the surface area is represented by various anatomic
parts (head and legs) changes with growth.
 Pa lm Met hod : used to estimate percentage of the

scattered burns; using the size of the px palm (abt. 1%
of body surface area) to assess the extent of burn
injury.
Ass essmen t
 Review the initial assessment data obtained by prehospital providers. Assess the
time of injury, mechanism of burn whether the burn happened in a closed space,
the possibility of inhalation of noxious chemicals, and any related trauma.
 Focus on the major priorities of any trauma patient: ABC, disability, exposure,
and fluid resuscitation.
 Assess respiratory status as first priority (airway patency and breathing

adequacy)
 Note any increased hoarseness, stridor, abnormal respiratory rate, and depth, or
mental changes from hypoxia.
 Evaluate circulation (apical, carotid, and femoral pulse)
 Check V/S frequently, using an ultrasound device if necessary.
 Check peripheral pulses on burned extremities hourly; use Doppler as needed

Ass essmen t
 Review the initial assessment data obtained by perhospital providers
 Focus on the major priorities of any trauma patient (ABC)
 Assess respiratory status as first priority
 Note any increased hoarseness, stridor, abnormal respiratory rate and
depth or mental changes from hypoxia
 Evaluate circulation (apical, carotid and femoral pulses)
 Check V/S frequently
 Check pheripheral pulses on burned extremities hourly
 Monitor fluid intake and output measure hourly
 Arrange for patients with facial burns to be assessed for corneal injury
 Assess body temperature, body weight, hx of preborn weight,
allergies, tetanus immunization, past medical surgical problems,
current illnesses and use of medication
 Assess depth of wound and identify areas of full and partial thickness
injury
 Assess neurologic status
 Assess patient’s and family understanding of injury and treatment
Dia gnos is
 Impaired gas exchange r/t carbon monoxide poisoning, smoke inhalation,

and upper airway obstruction
 Ineffective airway clearance r/t edema and effects of smoke inhalation
 Fluid volume deficit r/t increased capillary permeability and evaporative fluid
loss from burn wound.
 Hypothermia r/t loss of skin microcirculation and open wound
 Pain r/t tissue and nerve injury and emotional impact of injury.
 Anxiety r/t fear and emotional impact of injury

1. Promoti ng Gas Exc hanage and Air way Cl earan ce
 Provide humidified oxygen, and monitor arterial blood gas (ABGs), pulse
oximetry, and carboxyhemoglobin levels
 Assess breath sound, respiratory rate, rhythm, depth, and symmetry;
monitor for hypoxia.
 Observed for sign of inhalation injury: blistering of lips or buccal mucosa
 Report labored respiration, decreased depth of respirations; prepare to
assist with intubations and escharotomies
 Monitor patient with mechanical ventilation.
 Institute aggressive pulmonary care measures; turning coughing, deep
breathing, using spirometry and tracheal
suctioning.
 Maintain proper positioning t promote removal of secretions and patent
airway, optimal chest expansion.
 Maintain asepsis to prevent contamination of the respiratory tract and
infection, which increase metabolic requirements
2. Rest oring Flu id an d Ele ctr olyt e Bal an ce

 Insert large-bone IV catheter and indwelling urinary catheter
 Monitor V/S and urinary IO (hourly), note sign of hypovolimia or fluid
overload.
 Provide IV fluids as prescribe; document IO and daily weight.
 Elevate head of bed and burned extremities
 Monitor serum electrolyte levels (eg, sodium, potassium, calcium,
phosphorus, bicarbonate); recognizing developing electrolyte imbalance
3. Mai nta in ing Norma l Body Te mp er at ure

 Provide warm environment; use heat shield, space blanket, and heat
lights
 Assess core body temp. frequently
 Work quikly when wounds must be exposed to minimize heat loss from
the wound
4. Mi ni mi zin g Pa in and An xi et y
 Use pain sclae to asses pain
 Perform respiratory assessment before giving analgesic agent to

nonventilated px.
 Admistered IV analgesic as prescribe and assess response to medication
 Assess px and family understanding of burn injury, coping strategies, family

dynamics, and anxiety levels.
 Provide emotional support, reassurance and simple explanation about

procedures
 Provide pain releif, and give antianxiety med if px remain highly anxious and
agitated.
5. Mon ito r an d Ma nagi ng Pote nti al Comp lica ti on s
 Ac ute Re spir atory Failu re : assess for increasing dyspnea. Stridor,
changes in respiratory patterns; monitor arterial blood gas (ABGs),
pulse oximetry to detect problematic oxygen saturation and increasing
carbon monoxide; monitor chest x-rays for cerebral hypoxia
 Dis tri bu tiv e Shock : monitor for early signs of shock or progressive
edema. Administered fluid resuscitation as ordered in response to
physical findings; continue monitoring fluid status
 Ac ute Re nal Fa ilu re : monitor and report abnormal urine output and
quality
 Com pa rtme nt Syndr ome : assess nuerovascular status of extremities
hourly; report any extremity pain, loss of peripheral pulse or sensation
 Paralyt ic Ileu s: NGT and maintain in low intermittent suction until
bowel sound resume
 Cu rli ng’ s Ulce r: assess gastric aspirate for blood and pH; assess
stools for occult blood; administerd antacids and histamine blockers
(eg, ranitidine, (zantac)) as prescribed.
Acu te and In term edi ate P ha se
 It b egins 42 to 72 hours aft er t he b urn inju ry. Burn wo und care and
pai n cont ro l are the p riori ties i n thi s st ag e
Assessment
- Focus on hemodynamic changes
- Measure V/S frequently
- Assess peripheral pulses frequently
- Observe electrocardiogram for dysrhythmias resulting from potassium
imbalance
- Assess residual gastric volume and pH in px with NGT
- Note and report blood in gastric fluid or stool.
- Assess wound: size, color, eschar, exudate, abscess formation under the
eschar, epithelial buds, bleeding granulation tissue appearance
- Focus on pain and psychosocial response
- Assess for excessive bleeding adjacent to areas of surgical exploration
and debridement
Dia gnos is
 Excessive fluid volume related to resumption of capillary integrity
 Risk for infection related to loss of skin barrier and impaired immune
response
 Impaired skin integrity related to open burn wounds
 Imbalance nutrition: Less than body requirements
 Impaired physical mobility r/t burn wound edema, pain, and joint
contractures
 Ineffective coping r/t fear and anxiety
 Deficit knowledge about the burn treatment

1. Re sto ri ng Fl ui d Balanc e
 Monitor IV and oral fluid intake
 Measure IO and daily weight
 Report in changes in hemodynamic
 Administered low dose of dopamine as prescribe to increase perfusion and diuretics to
promote increased urine output
2. Prevent ing inf ection

 Provide a clean and safe environment
 Caution px to avoid touching wounds or dressings, bathed unburned areas and change
linens regularly
 Closely scrutinized wound t detect early sign of infection
3. Maint ain A deq uat e Nut ri tion

 Initiate oral fluid slowly when bowel sound resume
 Collaborate with dietitian
 Document caloric intake
 Weight px daily and graph weights
 Encourage px with anorexia to increase food intake, provide pleasant surroundings
4. Promot e Sk in Int eg ri ty
 Asses wound status
 Support px during distressing and painful wound care
 Coordinate complex aspects of wound care
 Assess and record any changes and progress in wound healing
 Assist, instruct, support, and encourage px and family to take part in dressing
changes and wound care.
5. Re lievi ng Pai n and Dis co mfo rt

 Teach px relaxation technique
 Use guided imagery to alter px perception and responses to pain
 Administer minor antianxiety med and analgesic agent before becomes too severe
 Promote comfort during healing phase
6. Promot ing Mob ili ty

 Prevent complications for immobility
 Modify intervention to meets patient’s need
 Make aggressive effort to prevent contractures and hypertrophic scaring of
the wound area after wound closure for a year or more
 Initiate passive ROM
 Apply splits or functional devices to extremities for contracture control
7. Moni tori ng and Manag ing Po tential Co mplic at ion

 Heart failure: assess for decreased cardiac output. Oliguria,edema, or onset
of S3 or S4 heart sound
 Pulmonary edema: assess fro increasing central venous pressure (CVP)
 Sepsis
 ARDS
 Visceral damage (frm electrical burns)
Rehabi litatio n an d Lon g-Te rm
Ph ase
Re habil ita ti on ph ase sh ou ld begi n imm edia te ly after th e bu rn has
occ urr ed .
Asse ssmen t
 Obtain information about patient’s educational level, occupation, leisure

activities, cultural background, religion and family interactions
 Assess self-concept, mental status , emotional response to injury and

 hospitalization, level of intellectual functioning, previous hospitalization,
response to pain and pain relief measures and sleep pattern
 Perform ongoing assessments relative to rehabilitation goal
 Document participation and self care abilities in wound care and ambulation
 Maintain comprehensive and continuous assessment for detection of early

complication
Dia gnos is
 Activity intolerance r/t to pain on exercise, muscle wasting,

and limited endurance
 Disturbed body image r/t altered appearance and self-

concept
 Deficient knowledge of postdischarge home care and follow-

up needs
1. Pr omo ting Activi ty Toler an ce

 Schedule care to allow periods of uninterrupted sleep
 Administer hypnotic agents as prescribed
 Communicate plan of care to family and other caregivers
 Reduce metabolic stress by relieving pain, preventing chilling or
fever and promoting integrity of all body systems to help conserve
energy
 Incorporate physical therapy exercises to prevent muscular atrophy
and maintain mobility required for daily activities
 Support positive outlook and increase tolerance for activity by
scheduling diversion activities in periods of increasing duration
2. Imp rovi ng Body Imag e and Sel f-Co ncep t
 Refer patient to support group to develop coping strategies
 Assess patient’s psychosocial reactions
 Support patient through small gestures
 Teach patient ways to direct attention away from a disfigured body to the
self within
 Coordinate communications of consultants
3. Mo nit oring and ma na gin g poten tial compl ica ti on

Contr actu res
 Provide early and aggressive physical and occupational therapy
 Support patient if surgery is needed to achieve full ROM
Impa ir ed ps yc hologi ca l adapt ation to th e bu rn in ju ry

 Obtain psychological or psychiatric referral as soon as evidence of major
coping problems appears
Dia betes M ellit us
 -Diabetes Mellitus is a group of metabolic disorders characterized by elevated

blood glucose hyperglycemia) resulting from defects in insulin production and
secretion, decreased cellular response to insulin, or both.
 -This leads to hyperglycemia, which may lead to acute metabolic

complications, such as diabetic ketoacidosis (DKA),and hyperglycemic
hyperosmolar nonketonic syndrome (HHNS)
 -Long term hyperglycemia may contribute to chronic microvascular

complications (kidney and eye disease) and neuropathic complications
 -Diabetic is also associated with an increased occurrence of CAD, CVA, and

peripheral disease
Ty pes of D ia betes
1. Type 1 (Form erl y Insul in-D epen dent D iabetes Me lli tus)
 About 5%-10% of diabetic patient have type 1 diabetes. Beta cells of the
pancreas that normally produce insulin are destroyed by an autoimmune
process. Insulin injections are needed to control the blood glucose
 Type 1 diabetes has a sudden onset, usually before the age of 30 years
2. Type 2 (Form erl y Non -I ns ulin -D ependent Diab etes Mell it us )
 About 90%-95% of diabetes has type 2 diabetes. Results from a decreased
sensitivity to insulin (insulin resistance) or from a decreased amount of insulin
production
 First treated with diet and exercise, then oral hypoglycemic agents as needed
 Occurs most frequently in patients older than 30 years of age and in obese
patients
3.G esta ti on al D iabete s
 Characterized by an degree of glucose intolerance with onset during
pregnancy (second or third trimester)
 It occurs in women 25 years of age or older, women younger than 25 years of
age who are obese, women with a family history of diabetes
 Polyuria, polydipsia and polyphagia
 Fatigue and weakness, sudden vision changes, tingling or numbness in

hands or feet, dry skin, sores that heal slowly and recurrent infections
 Onset of the type 1 diabetes may be associated with the nausea,

vomiting, or stomach pains
 Type 2 diabetes results from slow, progressive glucose intolerance and

results in long-term complications if diabetes goes undetected for many
years. Complications may have developed before the actual diagnosis is
made
 Signs and symptoms of DKA include abdominal pain, nausea, vomiting,

hyperventilation, and fruity breath odor.
As sess men t an d D ia gn osti c
Meth od s
 High blood glucose levels: fasting plasma glucose levels 126 mg/dL or more, or
random plasma glucose levels more than 200 mg/dL on more than one
occasion
 Evaluation for complications
Pr even tio n
 For obese patients(especially those with type 2 diabetes): weight loss is the
key to treatment and the major preventive factor for the development of
diabetes
Managemen t
 Primary treatment of type 1 diabetes is insulin.
 Primary treatment of type 2 diabetes is weight loss
 Exercise is important in enhancing the effectiveness of insulin
 Use of oral hypoglycemic agents if diet and exercise are not successful
in controlling blood glucose levels. Insulin injections may be used in
acute situations
 Because treatment varies throughout course because of changes in

lifestyle and physical and emotional status as well as advances in
therapy.
 Maintain fluid and electrolytes balance.
 Improve nutritional intake
 Reduce anxiety
 Monitor and Manage potential complications
 Teaching patient about self care

Dia betic Ket oacid os is
 Caused by an abs ence of in ade qu ate amou t of in su li n. This
res ult s in di sor der s in th e met abol is m of ca rboh ydr ates , prote in ,
and fat.
The three main clinical features of DKA :
(5) Hyperglycemia, due to decreased use of glucose by the cells and increased
production of glucose by the liver;
(7) Dehydration and electrolyte loss, resulting from polyuria, with a loss of up to
6.5 liters of water and up to 400 to 500 mEq each of sodium, potassium, and
chloride over 24 hours; and
(9) Acidosis, due to an excess breakdown of fatty acids and production of ketone
bodies, which are also acids. Three main causes of DKA are decreased or
missed dose of insulin, illness or infection, and initial manifestation of
undiagnosed or untreated diabetes.
Clin ica l M anifes tatio ns
 Polyuria, polydipsia (increased thirst)
 Blurred vision, weakness, and headache
 Orthostatic hypotension in patient with the volume depletion
 Weak rapid pulse
 GI symptoms, such as anorexia, nausea/vomiting, and abdominal

pain
 Acetone breath
 Kaussmauls respiration
 Mental status changes

As sess men t an d D ia gn osti c
Fi ndin gs
 Blood glucose level:300-800mg/dL
 Lower serum bicarbonate level: 0-15mEq/L
 Low pH: 6.8-7.3
 Low pCO2: 10-30 mmHg
 Low sodium and potassium
 Elevated creatinine, BUN, hemoglobin, and hematocrit

 Administer fluid as ordered
 Monitor fluid volume status
 Monitor for sign of fluid overload
 *Monitor carefully for hypokalemia due to rehydration and insulin treatment.
 Promote electrolyte and acid-base balance
 -Observe frequently for signs of hyperkalemia (ie, tall, peaked T waves on the
ECG) and obtain frequent (every 2-4 hours) potassium values during first 8
hours of treatment.
 Teach the patient about “sick-day rules” which are strategies to help
prevent diabetic complications.
 Do not eliminate insulin doses when nausea and vomiting occur
 Take usual insulin dose or previously prescribed sick-day doses and attempt to
consume frequent small portions of carbohydrates
 Drink fluids every hour to avoid dehydrations
 Check blood glucose level every 3-4 hours
End of the slides
Hepatic En ce phalop ath y
 ammonia (cerebral toxin)
 It is a potentially reversible neuropsychiatic abnormality

in the setting of liver failure.
 It can be diagnosed only after exclusion of other

neurological, psychiatric, infectious and metabolic
etiologies
Early signs:
 minor mental changes and motor disturbance
 Slight confusion and mood alteration
 Patient is unkempt
 Disturbance in sleep pattern (sleeps during the day)
 Restlessness and insomnia at night
As coma progresses the px may be difficult to awaken.

 asterisxis (flapping tremor of the hand)
 Reflexes are hyperactive; with worsening encephalopathy reflexes
disappear and extremities become flaccid
 Slowing and increase in amptitude of brain waves (EEG)
 Fetor hepaticus: breath odor like freshly mowed grass, acetone or old
wine
 Gross disturbances of consciousness and complete disorientation
 With further progression, frank coma and seizure occurs
Dia gnos is
 Liver enzymes- All increase
 SGPT (ALT)
 SGOT (AST)
 Serum cholesterol & ammonia increase
 Indirect bilirubin increase
 CBC – pancytopenia
 PTT – prolonged
 Hepatic ultrasonogram – fat necrosis of liver lobules

 Administer lactulose (cephulac) to reduce serum ammonia level
 Reduce protein intake
 Give enema as prescribed to reduce ammonia absorption from GIT
 Administer nonabsorbable antibiotics (neomycin) as an intestinal antiseptic
 Monitor serum ammonia level daily; monitor electrolyte status and correct if
abnormal
 Discontinue medications that may precipitate encephalopathy (eg, sedative

medication, tranquilizers, analgesic agents)
 Other treatment include administration of IV glucose, vitamins and oxygen

 Assess neurologic status frequently. Keep daily record of

handwriting and performance in arithmetic to monitor mental
status
 Monitor fluid IO and body weight daily
 Monitor for peritoneal, pulmonary, or other infection
 Instruct family to observe subtle sign of recurrent encephalopathy
 Maintain low protein, high calorie diet
End of the slides

En d- St age R enal
Dis eas e
Chronic renal failure or ESRD is a progressive irreversible

deterioration in renal function in which the body’s ability to
maintain metabolic and fluid and electrolyte balance fails,
resulting in uremia and azotemia
CAUSE S
 Diabetes mellitus
 Hypertension
 Chronic glomerulonephritis
 Pyelonephritis
 Obstruction of the urinary tract
 Hereditary lesions (eg. Polycystic kidney disease)
 Vascular disorder
 Infections
 Medications / toxic agents
 Environmental and occupational agents (eg. Lead, cadmium, mercury, chromium)

Pathop hysiolog y
Renal function declines
End product of CHON metabolism

accumulates in the blood
Uremia develops
Affects every system in the body

St ages of Kid ney Fa ilu re
Sta ge I - (Redu ced ren al res erv e)
 Loss of nephron function (40% - 70%)
 Px usually does not have sx because the remaining nephrons are able to carry
out the normal function of the kidney
Sta ge II - (Re nal in suffici en cy )

 Nephron function is lost (75% - 90%)
 Serum creatinine and blood urea nitrogen rise
 Kidney loses it’s ability to concentrate urine and anemia develops
 Px may report polyuria and nocturia
Sta ge III - (ES RD )

 Final stage of chronic renal failure
 Loss of nephron function (10%)
 All of the normal regulatory, excretory and hormonal function of the kidney are
severely impaired
 Elevated creatinine and BUN levels as well as electrolyte imbalances
 Dialysis is indicated
 Ca rd iva scu la r : hypertension, pitting and periorbital edema, pericardial friction rub,
pericardial tamponade, hyperkalimia
 Integu me ntary: ecchymosis, purpura, thin brittle nails, coarse thinning hair, gray-bronze
skin color, dry flaky skin
 Pulmonary: crackles, thick tenacious sputum, depressed cough reflex, shortness of

breath, tachypnea, kussmaul type of respiration, uremic pneumonitis
 Ga str oin test in al: ammonia odor of breath, metallic taste, mouth ulceration and
bleeding,N/V, constipation or diarrhea, bleeding in GIT
 Nu er ologic : weakness, fatigue, confusion, disorientation, tremors, seizure, burning of sole

of feet, behavioral change
 Musculos kel eta l: muscle craps, loss of muscle strength, renal osteodystrophy, bone
pain, fracture, foot drop
 Rep rodu cti ve: amenorrhea, testicular atrophy, infertility, decrease libido
 Hem atologic : anemia,thrombocytopenia

As sess men t an d D ia gno stic
Fi nd ings
1. Gl omeru lar filt ration rate
 24ᵒ urinalysis for creatinine clearance = decrease GFR
 Increase BUN level
 Serum creatinine (most sensitive indicator of renal function
2. Na and H2O rete ntion

 Kidney cannot concentrate or dilute urine normally
 Retain Na and H2O = increase risk for edem, heart failure and HPN
 Other px tends to lose salt and develop hypotension and hypovolemia
 Vomiting and diarrhea may produce Na and H2O depletion which worsen the uremic state
3. An emia
 Inadequate erythropoietin production
 Producing fatigue, angina and shortness of breath
4. Ca a nd Phosp or ous imb alanc e

 Body does not normally respond to the increased secretion of parathormone
 Active metabolite of vitaminD normally manufactured by the kidney decreases
 Uremic bone disease develops from the complex changes in Ca, PO4 and parathormone
balance
1. Me di cat io ns
 Antihypertensive - to manage HPN
 An ti sei sure agen ts - ( Diazepam, Phenytoin)
 Er yt hropo iet in (Epoge n ) - to manage anemia

Administer via IV or SubQ tid
A/E: HPN, increased clotting of vascular access
sites, seizure and depletion of iron stores
 Iron suppl em ent
 PO4 bi ndi ng agen ts - suitable for or select not to participate in dialysis or

transplantation
 Antacids
 Hyperphosphatemia and hypocalemia are treated with aluminium based antacid
 Magnesium based antacid should be avoided to prevent magnesium toxicit
2. Di et ther ap y
 Vitamin supplementation
 CHON restriction
 Potassium restriction
 Adequate caloric intake
 Fluid intake to balance fluid loses
 Na intake to balance Na loses
3. Dial ys is
 Used to remove fluid and uremic waste products from the body when the kidney cannot
do so.
 Used to treat px with edema that does not respond to tx, hepatic coma, hyperkalemiam
hypercalcemiam HPN and uremia
Ty pes of D ia lys is
 Meth ods of Thera py Complication includes:
1. Hemod ial ysis  Hypertriglyceridemia

 Commonly used method of  Heart failure
dialysis  Coronary heart disease
 Used for acutely ill and require
short term dialysis (days to weeks)
 Angina pain
 Used for ESRD who require long
 Stoke
term or permanent therapy to  Peripheral vascular
prevent death insufficiency
 Uses dial yz er (synthetic  Hypotension
semipermeable membrane  Painful muscle cramping
replacing the renal glomeruli and  Exsanguinations
tubules as the filter for the
impaired kidneys)
 Dysrhythmias
Dialysis disequilibrium
 Air embolism
 Dialysis disequilibrium
Hemod ia ly sis
Nu rs in g Dia gnos is
 Excess fluid volume r/t decreased urine output, dietary excesses

and retention of Na and H2O
 Imbalance nutrition: less than body requirements r/t anorexia,

N/V, dietary restriction and altered oral mucous membranes
 Deficient knowledge regarding condition and tx regimen

 Activity intolerance r/t fatigue, anemia, retention of waste product
and dialysis procedure
 Low self-esteem r/t dependency, role changes, change in body

image and sexual dysfunction
 Assessing fluid status and identifying potential source of imbalance
 Implementing dietary program to ensure proper nutritional intake
 Promoting positive feelings by encouraging increase self-care and

greater independence
 Report the health care provider the s/sx of decreased renal fxn
 Worsening s/sx of renal failure (N/v, change in usual output, ammonia

odor or breath
 s/sx of hyperkalemia
 s/sx of access problem (clotted fistula or graft and infection)
 Multiple dietary restrictions is required, including fluid intake, NA, K

and CHON restriction
End of the slides
PUL MONARY
EDE MA
Pulmon ary Ed ema
 Defined as abnormal accumulation of fluid in the lung tissue

and alveolar space
 Fluid may accumulate in the interstitial spaces.
 It is a severe life threatening condition.
CAUSES:
• Hypovolemia
• Sudden increased in intravascular pressure in the
lung
• Inadequate liver function
Pathop hysiolog y
pulmonary edema most commonly occurs as a result of increased

microvascular pressure from abnormal cardiac function
an acute event that results from HF, It can occur acutely,

such as with MI, or it can occur as an exacerbation of chronic HF
The backup of blood into the pulmonary vasculature resulting from

inadequate
left ventricular function causes an increased microvascular pressure
and fluid begins to
leak into the interstitial space and the alveoli.
 Decreased cerebral oxygenation
 Sudden onset of breathlessness
 Patient hands become cold and moist the nailbeds are cyanotic
 Neck veins are distended
 Very anxious and often agitated
 Confused and stuporous
 Pink foamy or frothy secretions by blood tinged

Pulmon ary Ed ema
Ass essmen t
 Auscultation reveals crackles in the lung bases that rapidly progress

toward the apices of the lungs.
 Crackles are due to the movement of air through the alveolar fluid
 Chest x-ray reveals increased interstitial marking
 Tachycardia, the pulse oximetry values begins to fall and arterial blood
gads analyzing demonstrates increased hypoxemia
Med ica l man agemen t
 Improving ventricular function and increased

respiratory exchanged
 Goal mgt. Accomplish through a combination of

oxygen medical therapies and nursing support.
Pulmon ary Ed ema
Ph arm acolog ic M anagemen t
1.Ox yg en thera py
 oxygen administered in concentration adequate to relieve hypocemia and
dyspnea
2. Morp hin e
 administered intravenously in small doses(2-5mg) to reduce peripheral
resistance and venous return so that blood can be redistributed from the
pulmonary circulatiuon to the parts of body.
3. Diu ret ic s
 promote the excretion of sodium and water by the kidneys
4. Dobutamin e
 intravenous medication given to patient with significant left ventricular
dysfunction.
5. Mi lri non e
 a phospodieterase inhibitor that delays the released of calcium from
intracellular reservoir and prevents the uptake of extracellular calcium by the
cells.
6. Ne siri ti de
 indicate for acutely decompensate HF
Nu rs in g ma nagemen ts
 Administration of oxygen and intubation and mechanical ventilation

if respiratory failure occurs.
 Positioning the patient to promote circulation
 Monitor I and O
 Monitoring pulse rate and blood pressure
 Examining skin turgor and mucous membranes for signs of DHN.

 Assessment symptoms of fluid overload.
End of the slides

PULMON ARY
EMB OLI SM
Pu lmon ary E mbolis m
 Pulmonary Embolism refers to the obstruction of the base or one or more

branches of the pulmonary arteries by the thrombus (or thrombi) that
originates somewhere in the venous system or in the right side of the heart.
 Gas exchange is impaired in the lung mass supplied by the obstructed

vessel.
 Massive pulmonary embolism is life threatening and can cause death within
the first 1 to 2 hours after the embolic event.
 It is a common disorder associated with trauma, surgery (orthopedic, major

abdominal, pelvic, gynecologic), pregnancy, oral contraceptive use,
congestive heart failure, age older that 50 years, hypercoagulable states,
and prolonged immobility. Most thrombi originates in the deep veins of the
legs.
Clinica l M anifes tation s
 Symptoms depend on the size of the thrombus and the area of the
pulmonary artery occlusion.
 Dyspnea is the most common symptom. Tachypnea is the most frequent sign
 Chest pain is common, usually sudden in onset and pleuritic in nature; it can
be substernal and may mimic angina pectoris
 Fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope,

shock, and sudden death may occur
 Multiple small emboli in the terminal pulmonary arterioles stimulate

symptoms of bronchopneumonia or heart failure
As sess men t an d D ia gno stic
Met hods
 Ventilation-perfusion scan, pulmonary

angiography, chest radiograph
 Electrocardiogram (ECG), tachycardia, PR interval

and T-wave changes, peripheral vascular studies,
impedance plethysmography, and arterial blood
gas (ABG) analysis (for hypoxemia)
Prev ention
 Ambulation or leg exercises in patients on bed rest
 Anticoagulant therapy before abdominothoracic

surgery and every 8 to 12 hours until discharge
from hospital
 Application of intermittent pneumatic leg

compression devices
 Stabilize the cardiorespiratory system
 Nasal oxygen is administered immediately to relieve hypoxemia, respiratory

distress, and cyanosis
 An infusion is started to establish an intravenous route for drugs or fluids
 Pulmonary angiography, spiral CT, perfusion lung scans, hemodynamic

measurements, and ABGs are performed
 An indwelling urethral catheter is inserted to monitor urinary output
 Infusion of dobutamine or dopamineECG is monitored continuously for

dysrhythmias and right ventricular failure
 Administration of digitalis glycosides, intravenous diuretic, and antiarrythmic

agents
 Administer small doses of intravenous morphine are given to relieve anxiety,

Anti coa gu lation Ther apy
 The partial thromboplastin time (PTT) is maintained at 1.5 to 2.5 times normal,
prothrombin time (PT) 1.5 to 2.5 time normal, or an ANR of 2.0 to 3.0
 Heparin id administered for 5 to 7 days
 Warfarin (Coumadin) is begun within 24 hours following the start of heparin
therapy and continued for 3 to 6 months
Throm boly ti c Thera py

 Thrombolytic therapy may include urokinase alteplase, anistreplase and
streptokinase (tissue plasminogen activator). It is reserved for pulmonary
embolism affecting a significant area and causing hemodynamic instability
 Bleeding is a significant side effect; nonessential invasive procedures are voided
Surgi ca l Managem ent

 Embolectomy by means of thoracotomy with cardiopulmonary bypass technique
 Transvenous catheter embolectomy with or without insertion of an inferior vena
caval filter (eg. Greenfield)
Nu rs in g In ter ven tion s
 Providing general care.. Encourage deep-brathing exercises
 Preventing thrombus formation. Encourage ambulation
 Monitoring anticoagulant and thrombolytic therapy. Advise bed rest,

monitor VS every 2 hours, limit invasive procedures
 Minimizing chest pain, pleuritic. Administer analgesics as prescribed for

severe pain
 Alleviating anxiety. Encourage patient to express feeling and concerns
 Managing oxygen therapy. Assess for hypoxia
 Providing postoperative nursing care. Measure pulmonary arterial

pressure and urinary output
THANK YOU!
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BI OLOG IC CRI SI S

Dr. Anthony Toledo MD,RN

ARRHYTHMIAS KIDNEY FAILURE (ERDS)

HEART BLOCK/STROKE PULMONARY EDEMA

BURNS PULMONARY EMBOLISM

 A condition in which systemic BP is adequate to

 Maintenance of tissue perfusion depends on

 Widespread serious reduction of tissue

 Loss of circulating volume due to excessive

 Most common type of shock.

 Characterized by decreased intravascular

Fl ui d and Bl ood re plac ement :

Red ist ri but ion of Flui ds

 Assist with fluid replacement

 Ensure safe administration of of prescribe fluids and

 Monitors and report signs of complications and effect of

 Monitor for cardiovascular overload and pulmonary edema:

 The ability of the heart to pump blood is impaired

 Causes of cardiogenic shock are either coronary or

 Coronary cardiogenic shock is more common and

 Noncoronary causes include tension pneumothorax,

 Dysrhythmias are common and result from a decrease in

 Cerebral hypoxia and manifested by confusion and agitation.

 Deceased urinary output and cold clammy skin.

 Coronary cardiogenic shock is treated with thrombolytic theraphy,

 Preventing cardiogenic shock

 Administering meds and IV fluids

 Maintaining mechanical devices

 Enhancing safety and comfort

 Result from profound vasodilation

 Three classification of distributive shock:

 The most common type of distributive shock,

 Gram-negative bacteria are the most common

 Gram-positive bacteria and viruses and fungi,

 Microorganism invasion causes immune response that

 There is an increase in the capillary permeability, with

Late ph as e: Hypody nami c or Ir re vers ib le p hase

 Urine, blood, sputum, and wound drainage specimens

 Begins immediately a broad-spectrum antibiotic

 Fluid replacement and aggressive nutritional

 Monitor for sign of infection at intravenous lines, arterial and venous

 Administered prescribed intravenous fluids and medications

 There is loss of vasomotor tone that

 Spinal cord injury

 Restoring sympathetic tone

 Immobilize the patient ( in spinal cord injury )

 Elastic compression stockings

 Heparin / low molecular weight heparin

 Pneumatic compression of the legs

 An antigen-antibody reaction brought about by

 Rremoval of causative agent

 Restore vascular tone ( epinephrine )

 Antihistamines and bronchodilators

 Assess for previous hypersensitivity reactions

 Prevention of future exposure to antigens

 Identification of new antigens

INITI AL STAG E / C OMP EN SATED / NONPR OGRESS IVE

 BP is maintained within normal limits due to the effect

 Blood loss less than 10%

 Apprehension and restlessness ( 1st sign of

 Identify the cause of shock

 Monitoring tissue perfusion