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 What is Shock?

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 )
Classification of shock
A. HYPOVOLEMIC SHOCK
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%.
HYPOVOLEMIC SHOCK
Predisposing factors:

External:FluidLoss Internal:FluidShift

trauma a. hemorrhage
surgery b. burns
vomiting c. ascite
diarrhea d. peritonitis
diuresis e. dehydration
diabetes insipidus
 Medical Management
GOALS:
restore intravascular volume
redistribute fluid volume
correct the underlying cause
Fluid and Blood replacement:
Lactated Ringers 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.

Redistribution of Fluids
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
Pharmacologic Exam

Desmopressin
Insulin
Anti-emetic
Anti-diarreal
Nursing Management
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
Cardiogenic Shock
Cardiogenic Shock
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.
Pathophysio of Cardiogenic
Shock
Clinical Manifestation:

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.

Medical Management
correction of underlying cause
initiation of first line treatment

supplemental oxygen
controlling chest pain
selected fluids support
vasoactive medications
controlling heart rate
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.
Pharmacologic

Dobutamine
Dopamine
Anti-arrythemic meds
Nitroglycerine
Vasoactive meds
Nursing Management

Preventing cardiogenic shock

Administering meds and IV fluids

Maintaining mechanical devices

Enhancing safety and comfort

Distributive Shock / Vasogenic
Shock ( Circulatory Shock )

Result from profound vasodilation

Three classification of distributive shock:

Septic shock, Anaphylactic shock and
Neurologic shock
Septic Shock
Septic Shock

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
Risk factors:

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
Pathophysiology

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.
 Clinical Manifestation
First phase: Hyperdynamic or Progressive phase
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 phase: Hypodynamic or Irreversible phase

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
Septic Shock
Medical Management
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.
Nursing Management
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
NEUROLOGIC SHOCK / SPINAL
SHOCK

There is loss of vasomotor tone that

includes arteriolar and venous
dilatation .
Predisposing factors:

Spinal cord injury

Spinal anesthesia

Depressant meds

Hypoglycemia
Medical Management

Restoring sympathetic tone

Nursing Management
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
Anaphylactic Shock
Anaphylactic Shock

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.
Predisposing factors:

Drug sensitivity
Transfusion reaction
Bee sting allergy
Latex sensitivity
Medical Management

Rremoval of causative agent

Restore vascular tone ( epinephrine )

Antihistamines and bronchodilators

Nursing Management

Assess for previous hypersensitivity reactions

Prevention of future exposure to antigens

Identification of new antigens

Patient education
Stages of Shock

INITIAL STAGE / COMPENSATED / NONPROGRESSIVE SHOCK

BP is maintained within normal limits due to the effect

of normally functioning regulatory mechanisms

Blood loss less than 10%

Signs and Symptoms

Apprehension and restlessness ( 1st sign of

shock )
Increase heart rate
Cool, pain skin
Metabolic acidosis
Fatigue
Tachypnea
Mental status change
Medical Management

Identify the cause of shock

Correction of shock
Support of the regulatory
mechanisms
Nursing Management

Monitoring tissue perfusion

LOC
V/S
Urine output
Skin
Laboratory values
Reducing anxiety
Promoting safety
Progressive Stage /
Decompensated

Exhaustion of the compensatory mechanism

Myocardial depression

Increased capillary permeability

Signs and Symptoms
A. Respiratory effects
hypoxemia and hypercarbia
intense inflammatory response
decreased surfactant production
acute respiratory distress syndrome ( acute lung injury, shock
lungs, non cardiogenic pulmonary edema )

B. Cardiovascular effects
dyshrythmias
myocardial infraction
cardiac depression

C. Neurologic effects
decreased cerebral perfusion
mental status change
behavioral change
papillary dilation
Signs and Symptoms
D. Renal effects
MAP<80mmHg
Acute renal failure

E. Hepatic effects
Decreased blood flow
Less ability to perform hepatic functions

F. gastrointestinal effects
Decreased blood flow
PUD
Bloody diarrhea
Sepsis
Medical Management

Depends on the type of shock

Depends of the decompensation of the

organ systems
Irreversible Stage

Sever organ damage

Can no longer respond to treatment

Survival is less likely

Medical Management

Same with progressive stage

Nursing Management

Same with progressive shock

Moral support to the family

Ethical issue ( living will )

Assessments
A. Early stages
Restlessness, confusion
Increase RR and PR, respiratory alkalosis
Diaphoresis, cool clammy skin/warm, flushed skin in septic shock
Normal to decreased urine output, thirst, dry mucous membrane
Hypokalemia

B. Late stages
Shallow respiration, decreased BP, increased PR, hypothermia
Oliguria, Anuria
Hyperkalemia
Metabolic acidosis
Edema
Cool clammy skin- hypovolemic, cardiogenic and septic shock
Lethargy, dilated pupils
Decreased bowel sounds
Cyanosis
DIC
Interventions
A. Promoting fluids balance
Blood transfusions
IV fluids

B. Assisting with cardiac support

Intraaortic balloon pump ( IABP)
Medical anti-shock trousers
Modified trendelenburg position

C. Assisting respiratory support

O2 therapy
Mechanical ventilator
Deep breathing, coughing excercises
Suction as necessary
Interventions
D. Assisting with renal support
Monitor I and O, BUN and creatinine
Diuretics

E. Assisting with GI support

NGT
H2 blockers and antacids

F. Promoting safety
Soft restraints as needed
Practice strict asepsis
Prevent complications of immobility
Protect from chills
Drug Therapy
Vasoconstrictors: Norepinephrine / epinephrine,
dopamine, dobutamine
Vasodilators: Nitrates like nitroglycerine and
Isosorbide
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
Arrhythmias
Cardiac Arrhythmias

It is an abnormal electrical conduction

or automaticity causing changes in
the heart rate and rhythm.
Predisposing factors:
Congenital
Myocardial Ischemia
MI
Organic heart disease
Drug effect and toxicity
Conductive tissue degeneration
Electrolyte imbalance
Acid-base imbalance
Cellular hypoxia
Pathophysiology

Result in the disturbance in the excitability,

automaticity, or conductivity

Heart rate and rhythm are altered, reducing

cardiac output
 Assessment
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, (-)
hypotension respiration, no palpable
blood pressure
Diagnosis

ECG- change in heart rate, rhythm

Blood chemistry : electrolyte

imbalance
Normal Sinus Rhythm
Normal Sinus Rhythm
Occurs when the electrical impulse starts at the
regular rate and rhythm n the sinus node and travels at
through the normal conduction pathway
Characteristics:
Ventricular and atrial rate: 60 to 100 in
adult
Ventricular and atrial rhythm: Regular
QRS duration: Usually normal, but may be
regularly abnormal
P wave: Normal and consistent shape; always
in front of QRS
PR interval: Consistent interval between 0.12
and 0.20 seconds
P: QRS ratio 1:1
 Types of Sinus node
Dysrhythmias
A. Sinus Bradycardia
occurs when the sinus node creates an impulse
at a slower rate than normal.
Characteristics:
Ventricular and atrial rate: Less than 60 in
adult
Ventricular and atrial rhythm: Regular
QRS duration: Usually normal but may be
regularly abnormal
P wave: Normal and consistent
interval between 0.12 and
0.20 seconds
P: QRS ratio 1:1
Sinus Bradycardia
Management

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 Tachycardia
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:

Ventricular and atrial rate: Greater than

100 in the adult
Venticular and atrial rhythm: Regular
QRS duration: 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.
P: QRS ratio 1:1
 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
Management

It is usually directed at abolishing its

causes.

Calcium channel blockers and Beta-blockers

may be used to reduce the heart rate
quickly.
 Types of Sinus node
Dysrhythmias

C. Sinus Arrhythmias

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.
 Characteristics:

Ventricular and atrial rate: 60 to 100 in the adult

Ventricular and atrial rhythm: Irregular
QRS duration: Usually normal, but may be regularly
abnormal
P wave: Normal and consistent shape, always in front of
the QRS.
PR interval: 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.
 Atrial Dysrhythmias

A. Premature Atrial Complex

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.
Characteristics:
Ventricular and atrial rate: Depend on the underlying
rhythm
Ventricular and atrial rhythm: Irregular
QRS duration: The QRS that follows the early P wave is
usually normal, but it may be abnormal.
P wave: 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 interval: 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
Management

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.

PACs should be monitored for increasing frequency

Atrial Flutter
Atrial Dysrhythmias

B. Atrial Flutter
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.
Atrial Flutter
Characteristics:
Ventricular and atrial rate: Atrial range
between 250 and 400 ventricular rates usually
Range between 75 and 150
Ventricular and atrial rhythm: Usually
Regular
P wave: Saw toothed shape. These waves
referred to as F wave
PR interval; Multiple F waves may make it
difficult to determine the PR interval.
P: QRS ratio: 2:1, 3:1, or 4:1
Sign and Symptoms

Chest pain
Shortness of breath
Low blood pressure.
Management
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

Atrial Fibrillation
 Atrial Dysrhythmias
C. Atrial Fibrillation
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).
Characteristics:
Ventricular and atrial rate: Atrial rate is 300
and 600 in untreated atrial fibrilation
Ventricular and atrial rhythm: Highly irregular
QRS shape and duration: usually normal but
may be abnormal
P wave: No discernible P waves; irregular
undulating waves are seen and are referred to as
fibrillatory or waves.
PR interval: Cannot be measured
P: QRS ratio: many:1
 Management
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.

Atrial Fibrillation
 Junctional Dysrhythmias
A. Premature Junction Complex
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 PACs

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.
Premature Junction
Junctional Dysrhythmias

B. Junctional Rhythm

Jucntional or idionodal rhythm occur when the AV

node, instead of the sinus node, become the
pacemaker of the heart.
Characteristics:
Ventricular and atrial rate: 40 to 60
Ventricular rhythm: Regular
QRS duration: Usually normal but may be
abnormal
P wave: May be absent, after the QRS complex,
or before the QRS; may be invented, especially in
lead II
PR interval: If P wave is in front of the QRS, PR
interval is less than 0.12 second
P: QRS ratio1:1 or 1:1
Junctional Dysrhythmias

C. Atrioventicular Nodal Reentry Tachycardia

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)
Characteristics:
Ventricular and atrial rate: atrial rate 150-250;
vent rate: 75-250
Ventricular and atrial rhythm: Regular; sudden
onset and termination of the tachycardia
QRS duration: Usually normal but may be
abnormal
P wave: usually very difficult to discern
PR interval: If P wave is in front of the QRS, PR
interval is less than 0.12 second
P: QRS ratio1:1 or 2:1
Ventricular Dysrhythmias
A. Premature Ventricular Complex

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.

PVCs may occur in regular sequence with normal rhythm.

Premature Ventricular
Complex
Characteristics:
Ventricular and atrial rate: Depend on the
underlying rhythm.
Ventricular and atrial rhythm: Irregular
QRS duration: 0.12 second or longer shape is
bizarre and abnormal
P wave: none
PP interval: 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
Management

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.
Ventricular Dysrhythmias
B. Ventricular Tachycardia

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
Characteristics:
Ventricular and atrial rate: 100to200
beat per minute
Ventricular and atrial rhythm: Usually
Regular
P wave: so atrial rate and rhythm may be
indeterminable.
PR interval: Very Irregular
P: QRS ratio: difficult to determine
Ventricular Tachycardia
Management

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.
Ventricular Dysrhythmias

C. Ventricular Fibrillation

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.
Ventricular Fibrillation
Characteristics:

Ventricular rate: Greater than

300 per minute
Ventricular and atrial rhytm:
Extremely irregular
QRS duration Irregular
 Management
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.
Ventricular Dysrhythmias

D. Idioventricular Rhythm
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

Characteristics:

Ventricular and atrial rate: Between

20and 40 if the rate exceeds 40, is known
(AIVR)
Ventricular and atrial rhythm: Regular
QRS duration: Bizarre, abnormal,
duration is 0.12 second or more.
Ventricular Dysrhythmias

E. Ventricular Asystole

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.
Ventricular Asystole
Management

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

HEART BLOCK
Conduction Abnormalities

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 Conduction
Abnormalities

A. First Degree Block

Occur when all the atrial impulse
are conducted through the AV node into
the ventricle at a rate slower than normal
Characteristics:
Ventricular and atrial rate: Depend on
the underlying rhythm.
Ventricular and atrial rhythm: Depend
on the underlying rhythm.
QRS duration; usually normal
P wave: In front of QRS complex; shows
sinus rhythm, regular shape.
P: QRS ratio1:1
First Degree AV Block
 Types of Conduction
Abnormalities
B.1 Second Degree Atrioventricular 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.
 Characteristics:
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; the RR interval characteristically reflect a pattern
of change .
QRS duration: Normal may be abnormal
P wave: In front of the QRS complex; shape depend on
underlying rhythm
PR interval: 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 Degree Atrioventricular
Block Type I
 Types of Conduction
Abnormalities
B.2 Second Degree Atrioventricular Block Type II

Occur when only some of the atrial impulses

are conducted through the AV node into the ventricles
Second Degree Atrioventricular Block
Type II
Characteristics:

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 of Conduction
Abnormalities

C. Third Degree Atrioventricular Block

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 .
Third Degree Atrioventricular
Block
Characteristics:
Ventricular and atrial rate: Depend on the
escape and underlying atrial rhythm.
Ventricular and atrial rhythm:The PP interval
is regular and the RR interval is regular; however
the PP interval is not Equal to the RR interval.
QRS duration: Depend on the escape of
rhythm
P wave: Depend on the underlying rhythm
P: QRS ratio: More P wave than QRS complexes
Management
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.
 Nursing Assessment
Major assessment include all possible cause of the
dysrhythmia and the dysrhythmias effect on the hearts
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
pulmonary disease ) may be also identified.
Nursing Assessment
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.
 Nursing Diagnosis
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
Nursing Intervention
1. Monitoring and managing the dysrhythmias

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.
Nursing Intervention
2. Minimize anxiety

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 clients controls and to make the unknown less
threatening.

3. Promoting Home and Community Based Care

Explain the importance of maintaining therapeutic serum levels of the

medications so that the patients understand why medications should be
taken regularly each day.
Adjunctive Modalities and
Management

Pacemaker therapy 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.
 Pacemaker Design and
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 hearts electrical activity through

a lead to the generator ; the generators 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.
Pacemaker Design and 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).
Clinical Manifestation

Block AV block usually 3 bundle branch

block
Symptomatic Bradycardia
Arrhythmia during surgery
Sick sinus syndrome
Nursing Intervention
Monitoring Pacemaker function- 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.

Prevent infections- changes the dressing

regularly and inspects the insertion site for redness,
swelling, soreness or any unusual drainage and
increase the temperature should be noted.
Nursing Intervention

Client teaching about pacemaker-

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
Stroke
Disruption of cerebral circulation that results in motor and sensory deficits

Causes:
Cerebral arteriosclerosis

Syphilis
Trauma
Hypertension

Thrombosis
Embolism
Hemorrhage

Vasospasm
Types of Stroke

1. Ischemic Stroke
Large Artery Thrombotic 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.

Small Penetrating Artery Thrombotic Strokes- affect one or

more vessels are the most common type of ischemic stroke. Also called
lacunar strokes. Occur in young ones.
Types of Stroke

Cardiogenic Embolic Strokes-

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.

Cryptogenic Stroke- which have no known cause and

other stroke from cause of cocaine used, coagulopathies, migraine
and spontaneous dissections of the carotid or vertebral arteries.
Clinical Manifestation
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 Manifestation
Motor loss
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 hemiplegia (paralysis of
one side of the body) due to the lesion of the opposite side of
the brain.
Hemiparesis or weakness of one side of the body
Flaccid paralysis and loss or decrease of deep tendon reflex.
Clinical Manifestation
Communication Loss

Dysarthia ( difficulty in speaking), caused by paralysis of the muscles

responsible for producing speech.

Dysphasia or aphasia (defective speech or loss of speech)

which can be expressive aphasia, receptive aphasia or global
(mixed) aphasia

Apraxia ( inability to perform a previously learned action) as may be

seen when a patient picks up a fork and attempts to comb.
 Clinical Manifestation
Perceptual Disturbance
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.
Sensory 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.
Clinical Manifestation
Sensory 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.
Clinical Manifestation
Cognitive Impairment

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.
Nursing Diagnosis
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.
Nursing Diagnosis

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

Diagnosic Test Findings
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
Brain scan: decreased perfusion
Digital subtraction Angiography:
occlusion or narrowing of vessel
Medical Management
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.
 Medical Management
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
 Nursing Intervention
1. Improving mobility and preventing joint deformities
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.
 Nursing Intervention
2 Preventing Shoulder pain
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

Nursing Intervention
3. Manage Dysphagia

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
STROKE
ISCHEMIC STROKE

HEMORRHAGIC STROKE
Hemorrhagic Stroke
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)
Hemorrhagic Stroke
Pathophysiology
Intracerebral hemorrhage

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

Intracranial (Cerebral) Aneurysm

Dilation of cerebral artery wall causes of weakness in the arterial walls.

An aneurysm due to atherosclerosis, vascular disease, head trauma or
advance aging.
Pathophysiology
Arteriovenous Malformation

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.

Subarachnoid Hemorrhage

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
Clinical manifestations
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.

 Assessment
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

Nursing Diagnosis
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.
 Medical Management
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.
 Nursing Intervention

Optimizing Cerebral Tissue Perfusion

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.
 Nursing Intervention
Implementing Aneurysm precaution

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 Homans sign report any abnormal findings

End of the slides

BURNS
Burns
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.
Medical Management
Four major goals relating to burn:
Prevention
Institution of life saving measure for the
severely burned person
Prevention of disability and
disfigurement
rehabilitation
 Pathophysiology
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 the Deep tissue can be
upper airways are the sites damaged by electrical
of tissue destruction burns or through
prolonged contact with a
heat source
increased fluid loss, infection,
hypothermia scarring
compromised immunity, and
changes in function, appearance,
and body image.
Classifications of Burn According
to Depth of Tissue Destruction

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.
First Degree Burn
Classifications of Burn According
to Depth of Tissue Destruction
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.
Second Degree Burn
Classifications of Burn According
to Depth of Tissue Destruction
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
Third Degree Burn
Extent of Body Surface Area
Injured
A. Inner zone
known as the area of coagulation, where cellular
death occurs
sustains the most damage.

B. Middle zone
has a compromised blood supply, inflammation, and
tissue injury.

C. Outer zone
the zone of hyperemia which sustains the least
damage.
RULE OF NINE
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

1st 8hrs give 50% of the formula

2nd 8hrs give 25% of the formula
3rd 8hrs give 25% of the formula
Methods in Determining the
Extent of Surface Area Burned
Rule of Nine: an estimation of the total body surface
area (BSA) burned by dividing the body into multiples of
nine.

Lund and Browder Method: 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.

Palm Method: 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.
 Assessment
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
Assessment
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 patients and family understanding of injury and treatment
Diagnosis
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
 Nursing Intervention
1. Promoting Gas Exchanage and Airway Clearance
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
Nursing Intervention
2. Restoring Fluid and Electrolyte Balance
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. Maintaining Normal Body Temperature

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
 Nursing Intervention
4. Minimizing Pain and Anxiety
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.
Nursing Intervention
5. Monitor and Managing Potential Complications
Acute Respiratory Failure: 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
Distributive Shock: monitor for early signs of shock or progressive
edema. Administered fluid resuscitation as ordered in response to
physical findings; continue monitoring fluid status
Acute Renal Failure: monitor and report abnormal urine output and
quality
Compartment Syndrome: assess nuerovascular status of extremities
hourly; report any extremity pain, loss of peripheral pulse or sensation
Paralytic Ileus: NGT and maintain in low intermittent suction until
bowel sound resume
Curlings Ulcer: assess gastric aspirate for blood and pH; assess stools
for occult blood; administerd antacids and histamine blockers (eg,
ranitidine, (zantac)) as prescribed.
Acute and Intermediate Phase
It begins 42 to 72 hours after the burn injury. Burn wound care and pain
control are the priorities in this stage

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
Diagnosis
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

Nursing Intervention
1. Restoring Fluid Balance
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. Preventing infection
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. Maintain Adequate Nutrition

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
Nursing Intervention
4. Promote Skin Integrity
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. Relieving Pain and Discomfort

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
Nursing Intervention

6. Promoting Mobility
Prevent complications for immobility
Modify intervention to meets patients 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. Monitoring and Managing Potential Complication

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)
Rehabilitation and Long-Term
Phase
Rehabilitation phase should begin immediately after the burn has
occurred.
Assessment

Obtain information about patients 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
Diagnosis

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
Nursing Intervention

1.Promoting Activity Tolerance

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
Nursing Intervention
2. Improving Body Image and Self-Concept
Refer patient to support group to develop coping strategies
Assess patients 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. Monitoring and managing potential complication

Contractures
Provide early and aggressive physical and occupational therapy
Support patient if surgery is needed to achieve full ROM

Impaired psychological adaptation to the burn injury

Obtain psychological or psychiatric referral as soon as evidence of major
coping problems appears
Diabetes Mellitus
-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
 Types of Diabetes
1. Type 1 (Formerly Insulin-Dependent Diabetes Mellitus)
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 (Formerly Non-Insulin-Dependent Diabetes Mellitus)
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.Gestational Diabetes
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
Clinical Manifestation
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.
Assessment and Diagnostic
Methods
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

Prevention
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
Management
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.
Nursing Management
Maintain fluid and electrolytes balance.

Improve nutritional intake

Reduce anxiety

Monitor and Manage potential complications

Teaching patient about self care

Diabetic Ketoacidosis
Caused by an absence of inadequate amout of insulin. This results
in disorders in the metabolism of carbohydrates, protein, and fat.

The three main clinical features of DKA :

(1) Hyperglycemia, due to decreased use of glucose by the cells and increased
production of glucose by the liver;

(2) 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

(3) 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.
Clinical Manifestations
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
Assessment and Diagnostic
Findings

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

 Nursing Management
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 Encephalopathy

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
Clinical Manifestation
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
Diagnosis
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

Medical Management
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

Nursing Management
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

End- Stage Renal Disease

Chronic renal failure or ESRD is a progressive irreversible

deterioration in renal function in which the bodys ability to
maintain metabolic and fluid and electrolyte balance fails,
resulting in uremia and azotemia
 CAUSES
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)

Pathophysiology
Renal function declines

End product of CHON metabolism

accumulates in the blood

Uremia develops

Affects every system in the body

 Stages of Kidney Failure
Stage I - (Reduced renal reserve)
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

Stage II - (Renal insufficiency)

Nephron function is lost (75% - 90%)
Serum creatinine and blood urea nitrogen rise
Kidney loses its ability to concentrate urine and anemia develops
Px may report polyuria and nocturia
Stage III - (ESRD)
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
 Clinical Manifestation
Cardivascular: hypertension, pitting and periorbital edema, pericardial friction rub,
pericardial tamponade, hyperkalimia

Integumentary: 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

Gastrointestinal: ammonia odor of breath, metallic taste, mouth ulceration and

bleeding,N/V, constipation or diarrhea, bleeding in GIT

Nuerologic: weakness, fatigue, confusion, disorientation, tremors, seizure, burning of sole

of feet, behavioral change

Musculoskeletal: muscle craps, loss of muscle strength, renal osteodystrophy, bone

pain, fracture, foot drop

Reproductive: amenorrhea, testicular atrophy, infertility, decrease libido

Hematologic: anemia,thrombocytopenia
 Assessment and Diagnostic
Findings
1. Glomerular filtration rate
24 urinalysis for creatinine clearance = decrease GFR
Increase BUN level
Serum creatinine (most sensitive indicator of renal function

2. Na and H2O retention

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. Anemia
Inadequate erythropoietin production
Producing fatigue, angina and shortness of breath

4. Ca and Phosporous imbalance

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
 Medical Management
1. Medications
Antihypertensive - to manage HPN

Antiseisure agents - (Diazepam, Phenytoin)

Erythropoietin (Epogen) - 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 supplement

PO4 binding agents - 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
 Medical Management
2. Diet therapy
Vitamin supplementation

CHON restriction

Potassium restriction

Adequate caloric intake

Fluid intake to balance fluid loses

Na intake to balance Na loses

3. Dialysis
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
Types of Dialysis
Medical Management
Methods of Therapy
Complication includes:
1. Hemodialysis
Commonly used method of Hypertriglyceridemia
dialysis Heart failure
Used for acutely ill and require Coronary heart disease
short term dialysis (days to weeks) Angina pain
Used for ESRD who require long Stoke
term or permanent therapy to
prevent death Peripheral vascular
insufficiency
Uses dialyzer (synthetic
semipermeable membrane Hypotension
replacing the renal glomeruli and Painful muscle cramping
tubules as the filter for the Exsanguinations
impaired kidneys) Dysrhythmias
Dialysis disequilibrium Air embolism
Dialysis disequilibrium
Hemodialysis
 Nursing Diagnosis

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
Nursing Management
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
PULMONARY
EDEMA
Pulmonary Edema
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
 Pathophysiology
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.
Clinical Manifestation
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

Pulmonary Edema
Assessment

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
Medical management

Improving ventricular function and increased

respiratory exchanged

Goal mgt. Accomplish through a combination of

oxygen medical therapies and nursing support.
Pulmonary Edema
Pharmacologic Management
1.Oxygen therapy
oxygen administered in concentration adequate to relieve hypocemia and
dyspnea
2. Morphine
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. Diuretics
promote the excretion of sodium and water by the kidneys
4. Dobutamine
intravenous medication given to patient with significant left ventricular
dysfunction.
5. Milrinone
a phospodieterase inhibitor that delays the released of calcium from
intracellular reservoir and prevents the uptake of extracellular calcium by the
cells.
6. Nesiritide
indicate for acutely decompensate HF
 Nursing managements

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

PULMONARY
EMBOLISM
Pulmonary Embolism
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.
Clinical Manifestations

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
Assessment and Diagnostic
Methods

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)
Prevention

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
Medical Management
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,

 Medical Management
Anticoagulation Therapy
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

Thrombolytic Therapy
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

Surgical Management
Embolectomy by means of thoracotomy with cardiopulmonary bypass technique
Transvenous catheter embolectomy with or without insertion of an inferior vena
caval filter (eg. Greenfield)
Nursing Interventions
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
END OF THE SLIDE

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