Glasgow Coma Scale – Patients with

low scores(3-4) have high mortality

and poor prognosis for cognitive
recovery compared to patients with
higher scores (8 and above)
Eye Opening
Spontaneously 4 Glasgow Coma Scale
To speech 3 Maximum score: 15
To pain 2
None 1
Verbal response
Oriented 5
Confused 4
Inappropriate 3
Incomprehensible 2
None 1
Motor Response
Obeys Command 6
Localizes pain 5
Withdraws (pain) 4
Flexion (pain) 3
Extension (pain) 2
None 1
P - Pattern
Q - Quality
R - Reaction
S - Severity
T - Treatment done
AMPLE Mnemonic For Multiple Trauma

A=Allergies,

M=Medication,

P=Past medical history,

L=Last food intake,

E=Events preceding the injury

A=Airway
B=Breathing
C=Circulation
D=Disability
E=Exposure
A=Is patient ALERT?
V=Is patient responding to VERBAL
stimulus?
P=Is patient responding to PAINFUL
stimulus?
U=Is patient UNCONCIOUS?
 Components Score
C - Circulation
Normal capillary refill and BP>=100
2
Delayed capillary refill or BP>=85<100
1
No capillary refill or BP<85 0

R - Respiration
Normal 2
Abnormal (labored or shallow)
1
Absent 0
A - Abdomen
Abdomen and thorax non-tender 2
Abdomen and thorax tender 1
Abdomen rigid or flail chest* 0

M - Motor
Normal 2
Responds only to pain
1
(other than decerebrate)
no response (decerebrate)
0
S - Speech
Normal 2
Confused 1
No intelligent words 0
Score <= 8: Major
Trauma
Score >= 9: Minor
Trauma
 Pericardium – loose fitting of the heart
composed of membranes and 5-20ml
fluid
 Cardiac layers – epicardium,
myocardium, endocardium
 Chambers – right and left atria; right
and left ventricles
 Valves –Tricuspid, bicuspid, semi-lunar
 Coronary circulation
Left coronary – LAD, LCA
Right coronary
S3 Gallop- ventricular overload; heard
after S2; “ken-tuck-y”
S4 Gallop- increased resistance to
ventricular filling; heard late in
diastole; “ten-ne-see”
Splitting heart sounds –Aortic and
pulmonic valve does not close
simultaneously
Systolic Murmur- turbulent blood flow
Ultrasound
Coronary angiography
Electrocardiogram
Serum Studies
CK-MB – (3-4 days)
LDH – Lactate dehydrogenase (7-14
days)
Troponin –T (14-21 days)
Aspartate Transaminase (3-4 days)
C- Reactive Protein
Myeloperoxidase
Intra-arterial blood pressure(80-90
60-65
mmHg)
Central venous pressure ( 1-8 mmHg or
4-12 cm water)
Pulmonary artery pressure ( 8-12
mmHg)
Cardiac output (4-8 L/min)
Venous oxygen Saturation (60-80%)
 Consent
 Explain procedure – cooperation
 Trendelenberg position – lower
extremity source
 Assist during procedure – local
anesthesia
 Instruct for deep breath and hold;
neck flexion for PICC
 Correct reading
 Sterile and Aseptic technique –
prevent infection.
Cannulation of central vein or arterial
wall
Pneumothorax and hemmorrhage
Infection by the indwelling invasive
device
Catheter occlusion
Ischemia distant to the site of catheter
Disturbance of cardiac rhythym
 BLOOD GASES:
ARTERIAL/VENOUS
Normal Arterial Venous
Values
pH 7.35-7.45 7.31 to 7.42

PO2 80 to 100 35 to 45

PCO2 35 to 45 39 to 52

HCO3 (mEqL) 22 to 26 22 to 26

Anion gap 10 to 18 8 to 16
(mEq/L)
 ANALYSIS OF ARTERIAL BLOOD GASES
COMPONE DESCRIPTION VALUES
NT Measures hydrogen ion (H+) 7.35-7.45
pH concentration
Increase in ions, acidosis <7.35
Decrease in ions, alkalosis >7.45
•Partial pressure of in CO2 arteries 35 to 45
•Respiratory component of acid- mmHg
base regulation
pCO2 Hypercapnia, respiratory acidosis
Hypoventilation, respiratory
>45 mmHg
<35 mmHg
alkalosis
•Measures serum bicarbonate Normal: 22 to
•May reflect primary metabolic 26 mEq/L
disorder or compensatory
HCO3 mechanism to respiratory acidosis
Metabolic acidosis <22 mEq/L
Metabolic alkalosis >26 mEq/L
The GOAL is to maintain alveolar ventilation, correct
hypoxemia and maximize O2 transport when client
cannot sustain spontaneous and effective respirations.

 Initiating Mech. Ventilation/ Setting up machine

1.Set up the machine
2. Plug to emergency outlet
3. Select ventilatory settings ( per doctor’s orders)

 Tidal volume, FiO2, peak inspiratory flow rate, Mode

( A/C, IMV, SIMV, PSV), Sensitivity, Pressure limit, I:E
ratio, respiratory rate.
Types of Ventilators
1. Pressure- Cycled
2. Volume- Cycled
3. Time- Cycled
Nursing Care
1.Note ETT position. Monitor cuff
pressure
2. Restrain only if needed
3. Administer sedatives prn.( To keep
patient calm)
4. Auscultate breath sounds
5. Monitor ventilator settings
6. Change tubings prn.
7. Perform CPT as needed
8. Monitor ABG, O2 sat. , V/S
9. Assess position change
10. Provide alternate communication
measures
11. Suctioning prn.
12. Respond to alarms
Weaning Parameters:

PaO2 is over 70-80 mmHg

PaCO2 = normal
Acceptable general respiratory status
 Correction of underlying problem
Description:
a visual representation of the
electrical activity of the heart
reflected by changes in the
electrical potential at the skin
surface
 R

P T U
Q
S
 R

P T U
Q
S
 R

P T U
Q
S
 R

P T U
Q
S
Leads 1,II, III, AVF, V6 – all waveforms
are upright
aVR – all waveforms are negatively
deflected
aVL – P and T are negative, QRS are
biphasic
V1,V2 – P and T positive, QRS
negative
V3, V4, V5 – P and T positive, QRS
biphasic
Atrial( 60-100 Bpm)
Junctional ( 40-60 Bpm)
Ventricular (30-40 Bpm and lower)

Ectopic Foci- may arise from any part

of the heart atria or ventricles
causing abnormal heart rates and
activity.
The following conditions can
interfere with normal heart
functioning:
A. Disturbances of rate or
rhythm
B. Disorders of conductivity
C. Enlarged heart chambers
D. Presence of myocardial
infarction
E. Fluid and electrolyte
imbalances.
 Each EKG should include identifying
information of patient
 The standard EKG is the 12-lead
EKG.
 Bedside monitoring through
telemetry is more commonly seen
in the clinical setting using 3-5
leads
 A portable continuous monitor
(Holter monitor) can be placed on
the client to provide a magnetic
tape recording; patient to record
 The EKG graph paper consists of
small and large squares:

A. The small squares represent 0.04

seconds with five of these small
squares combining to form one
large square.
B. Each large square represents 0.20
seconds (0.04 seconds x 5). Five
large squares represent 1 second.
 Using Boxes – 300-150-100-75-60
Calculation of heart rate using the
six-second rule:
1. The easiest means of calculating
the heart rate.
2. Can not be used when the heart
rate is irregular.
3. 30 large squares equal one-six
second interval.
4. Count the number of R-R intervals
1. P wave: atrial systole
A. Represents depolarization of the
atrial muscle
B. Should be rounded without
peaking or notching.
2. QRS complex: ventricular systole
A. Represents depolarization of the
ventricular muscle.
B. Normally follows P wave.
C. QRS interval measured from
beginning of the QRS to the end
T wave: ventricular diastole
1. Represents repolarization of
the ventricular muscle.
2. Follows QRS complex.
3. Usually slightly rounded
without peaking or notching.

U wave – a small wave following

the T-wave indicating
potassium depletion
1. ST segment:
A. Represents every ventricular
repolarization.
B. Measured from the end of the S
wave to the beginning of the T
wave.
2. PR interval:
A. Represents the time required for
the impulse to travel through the
atria (SA node), through the A-V
node, to the Purkinje fibers in the
ventricles.
B. Measured from the beginning of
the P wave to the beginning of the
QRS complex.
1. U wave:
A. Not always present.
B. Most prominent in the presence of
hypokalemia.
2. QT interval:
A. Represents the time required to
completely depolarize and
repolarize the ventricles.
B. Measured from the beginning of
the QRS complex to the end of the
T wave. (0.32-0.44 sec.)
3. R-R interval:
A. Reflects the regularity of the heart
rhythm.
Normal sinus rhythm (60-100)
Sinus bradycardia (below 60)
Sinus tachycardia (101-180)
Sinus arrhythmia (irregular)
Normal Sinus Rhythm
Look at the p waves:
rate is 60-100/min
cycle length do not vary by 10%
PR interval is 0.12 sec. or more

Lead II
Sinus Bradycardia

Regularly occurring PQRST

Rate < 60 / min

Rate = 48/min
Rate = 48/min
Sinus Tachycardia

Regularly occurring PQRST

Rate > 100 / min

Rate = 111/min Rate = 111/min Rate = 111/min

Sinus Arrhythmia
Identical but irregularly
occurring PQRST
longest PP or RR > the
shortest by 0.16 sec or more
Rate = 71/min
Rate = 94/min Rate = 94/min
Rate = 79/min
PAC – P waves are premature
Atrial tachycardia – (150-250) difficult
to distinguish P from T waves
Atrial flutter – atrial (250-450) no p
waves but replaced by saw-toothed
waves before a QRS
Atrial fibrillation- atrial (400-600)
bizzare P waves before a QRS
Premature Atrial Contraction

Prematurely occurring PQRTS complex

P wave different in configuration
from the sinus beat.
PR interval often long.
QRS narrow.
 Multifocal Atrial
Tachycardia
Impulses originate irregularly
and rapidly at different points
in the atrium
Varying P wave, PR, PP and RR intervals
Ventricular rate > 100/min
 Atrial Flutter

Atrial rate = 220-300/min

( P as flutter waves )
Variable degree of AV block
( irregular RR interval )
Atrial Fibrillation

No discernible P waves
Irregular RR interval
PVC – P wave absent with wide
Bizzare QRS
Ventricular Tachycardia- wide saw-
toothed QRS (200-250) without P or
PR
Ventricular Fibrillation- rate cannot be
determined, rapid and chaotic;
coarse or fine
Asystole- flat line
 Premature Ventricular Contraction
Prematurely occurring complex.
Wide, bizarre looking QRS complex.
Usually no preceding P wave.
T wave opposite in deflection to the QRS
complex.
Complete compensatory pause following
every premature beat.
Ventricular Tachycardia

At least 3 consecutive PVC’s

Rapid, bizarre, wide QRS complexes
(> 0.10 sec)
No P wave (ventricular impulse
origin)

Rate > 140 / min

Ventricular Fibrillation
Firstdegree AV – Normal rate and
rhythm with prolonged constant PR
interval
Second degree AV 1 or 2– Atrial
regular, ventricular irregular, more P
waves than QRS , PR lengthens then
drops a QRS periodically or QRS
maybe absent
Third degree AV - Atrial -ventricular
no relationship, more P waves than
QRS , No PR ; QRS narrow or wide
FIRST DEGREE
AV BLOCK
PR interval > 0.20 sec

0.28 sec 0.28 sec 0.28 sec

 Second Degree
Atrioventricular Blocks

Do you have a normal P wave? Yes

Do you have a normal PR segment? No
Do you have a normal PR interval? No
Will there be intermittent P waves not
followed by QRS complex? Yes (dropped beats)
 THIRD DEGREE
AV BLOCK
Complete atrioventricular block
Impulses originate at both SA node and at
the subsidiary pacemaker below the block
Do you have regularly occurring P waves and QRS complexes? Yes
Are the P waves related to the QRST complexes? No
Is the atrial rate < = > ventricular rate? greater

Ventricular rate = 83 BPM Ventricular rate = 83 BPM

Atrial rate = 100 BPM Atrial rate = 100 BPM

Atrial rate = 100 BPM
Frequent PVC’s, Salvo, V-tach -
Lidocaine to regulate rhythm to normal;
cardioversion
Asystole – epinephrine, atropine to
initiate rhythm and contractions, then
defibrillation if with pulse
Coarse V-Fibrillation with pulse –
defibrillation, then medications to
regulate rhythm
 Coronary Artery Disease
( CAD)-
loss of oxygen and nutrients to myocardial tissue
due to poor coronary blood flow. The most
common cause is atherosclerosis ( fatty, fibrous,
possibly calcium deposits in the lumen of
coronary arteries)
Risk factors: Non- modifiable/ non-controllable:
 Heredity
 Age ( above 40),
 Sex/gender( more men , more likely in women
who smoke and those on oral contraceptive)
 Race ( more in blacks)
• Diet
• Habit/ Lifestyle ( sedentary; smoking- risk drops
within 1 year of quitting)
• Contributing: Obesity, Response to stress, other
diseases like DM,
• Increased LDL ; decreased HDL; Hypertension;
• Coronary artery spasm associated with
atherosclerosis or from unknown cause
The mnemonic A B C D E to control risk
factors

A for aspirin and antianginal therapy,

B for beta-blocker therapy and BP control,

C for cigarettes and cholesterol,

D for diet and diabetes,

E for education and exercise.

 Angina/ Angina Pectoris-
a transient ischemic attack resulting
from decreased blood supply through
partially occluded coronary arteries.
Precipitating factors include: extreme
changes in temperature, physical
exercise, emotional factors, eating a
heavy meal, sexual intercourse,
valsalva maneuver, cigarette
smoking, stimulants.
 Percutaneous Transluminal Coronary
Angioplasty (PTCA), Coronary Artery Bypass
graft ( CABG), or Stress Test may cause angina.
 Pain or chest discomfort may be described as
burning, suffocating squeezing or crushing
tightness in the substernal or precordial areas
that radiates to the left arm ( or both), neck, jaw
or shoulder blade.
 Patient
may clench his fist or rub his left arm
when describing it. Commonly accompanied by
nausea, vomiting, fainting, sweating, and cool
extremities.
1. Stable ( chronic) Angina :
 usually precipitated by physical
exertion, emotional stress, or cold
weather.
 Has stable pattern of onset,
duration and severity and relieving
factors
 pain or discomfort may vary from
mild to severe and usually lasts for
1 to 5 minutes .
 Relieved with rest and sublingual
NTG, or both.
1. Unstable angina

 Preinfarction angina, crescendo

angina or intermittent coronary
syndrome
 Triggered by unpredictable degree
of exertion or emotion, which may
occur at night.
 It must be treated as a medical
emergency with the client
receiving immediate medical
attention
 Often described as progressive,
prolonged, or frequent angina with
increasing severity.
 Pain or discomfort is more intense
lasting up to 30 minutes, often arouses
patient from sleep.
 Pain is not completely relieved with
NTG, may require narcotics (like
Morphine Sulfate)
 Without significant EKG changes like ( T
wave inversion =Ischemia ) diagnosis is
based on history and clinical condition
 10-30% of clients progress to having an
MI in 1 year, and 29% die from MI in 5
years
1. Prinzmetal’s angina :
 Variant angina similar to classic angina ;
chest pain of longer duration; may occur
at rest
 Attacks tend to happen between midnight
and 8am
 Results from coronary artery associated
with elevation of ST segment in the EKG
 NTG generally yields quick relief.
 Calcium channel blockers ( Verapamil,
Nifedipine, Dialtezem ) are most effective
Goal: vasodilation and reduce myocardial
oxygen demands
 When administering Nitroglycerin: Take
baseline V/S, give it sublingually x 3 every 5
min. take V/S after each dosage.

 Ifthe BP is less than 100mmHg or less than

25mmhg lower than the previous reading, do
not give it, the nurse lowers the head of the
bed and notifies the physician

 ST segment depression and T-wave inversion

occur with chest pain and return to normal
when episode subsides; ST segment elevation
( Prinzmetal’s) which goes back to normal
when spasm subsides.
 Definition
1. Necrosis of myocardial cells is life-
threatening event
2. Loss of functional myocardium
affects heart ability to maintain
effective cardiac output
 Ulceration or rupture of complicated
atherosclerotic lesion
 Substances released which lead to platelet
aggregation, thrombin generation, local
vasomotor tone
 Formation of clot which occludes vessel and
blocks blood to myocardium distal to
obstruction
 Prolonged ischemia (>20 – 45 minutes):
irreversible hypoxemic damage
 Cellular metabolism shifts from aerobic to
anaerobic metabolism producing hydrogen
ions and lactic acid
Depth of Infarction
 Subendocardial or non-Q-wave infarction
1. Damage is limited to subendocardial
tissue
2.Occurs within 20 minutes of injury
3. Common complication is recurrent
ischemia
4. S-T segment depression with small
infarct
 Intramural infarction – in myocardium ;
associated with angina pectoris
 Transmural infarction or Q- wave
infarction
1.All layers of myocardium to epicardium
Pain: classic manifestation
Lasts > 15 – 20 minutes
Unrelieved by rest or nitroglycerine
Onset sudden and usually not
associated with activity
Described as crushing and severe; as
a pressure, heavy or squeezing
sensation; tightness or burning in the
chest
Location: center of chest (substernal)
and may radiate to shoulders, neck,
jaw, arms
Women and older adults have
atypical chest pain with complaints of
indigestion, heartburn, nausea,
vomiting
No chest discomfort in 25% of clients
with acute MI
Additional symptoms relate to
sympathetic nervous system
stimulation:
Cool, clammy, mottled skin
Tachypnea
Sense of impending doom and death
Depending on location and amount of
infarct
Hypertension or hypotension
Signs of heart failure
Nausea and vomiting, bradycardia
Hiccups
Sudden death (large blood vessel
involvement)
Treatment goals:

Relievechest pain
Reduce extent of myocardial damage
Maintain cardiovascular stability
Decrease cardiac workload
Prevent complications
Rapid assessment and early diagnosis
key:

“Time is muscle”
Initiation of definitive treatment
within 1 hour of entry into health care
system
Major problem: delay in seeking
medical care post onset of symptoms
(44% wait > 4 hours to seek
treatment)
Serum cardiac markers: Proteins
released from necrotic heart muscle;
ordered on admission and for 3
succeeding days
a. Creatine phosphokinase (CK)
Appears 4 – 6 hours postacute MI; peaks
12 –24 hours; declines over next 48 –
72 hours

b. CK-MB
Isoenzyme of CK most sensitive indicator
of MI
CK-MB elevation > 5% positive indicator of
Cardiac-specific troponin T (cTnT) and
Cardiac-specific troponin I (cTnI)

Proteins released during myocardial

infarction; sensitive indicators for
myocardial damage
Released and levels rise with necrosis
of cardiac muscle
Sensitive enough to detect very small
infarction and remain in blood 10 –
14 days post MI
Other laboratory tests
CBC, Erythrocyte Sedimentation
Rate: WBC and ESR elevated of
because of inflammation
Arterial
Blood Gases: assessment
secondary to physical effects of MI
Electrocardiography: T wave
inversion;
Elevation of S-T segment; Formation of
Q wave
Nursing Diagnoses:

Acute Pain
Ineffective Tissue Perfusion: obtain
12-lead ECG to assess significant
chest pain
Ineffective Coping: overuse of denial
may interfere with learning and
compliance with treatment
Fear
Nursing Interventions
2. Reliefof pain- MONA is the guide of
treatment of clients with chest pain.
M for Morphine sulfate,
O for Oxygen therapy,
N for nitrates and
A for aspirin.
2. Promote measures to maintain cardiac
parameters-
• Cardiac monitoring ( place client on Lead II),
• Report changes in LOC, Heart /Lung sounds,
• Peripheral pulses, Capillary refill time (less
than 3 sec),
• JVD (jugular vein distention),
• Monitor Pulmonary artery wedge
pressure( PAWP) if patient has a
Swan- Ganz catheter (PAWP less
than 18 mmHg shows volume
depletion and PAWP more than 18
mmHg signifies pulmonary
congestion or cardiogenic shock
• Monitor urinary output, Decreased
activity level, Schedule rest periods,
Adm. stool softeners.
Promote measures to maintain
adequate O2 and carbon dioxide
exchange
• O2 Administration,
• Pulse oximetry, Monitor ABG
results, Monitor secretions by
coughing and suctioning,
• Prepare for intubation as necessary.
Thrombolytics- agents which cause
lysis of a pathogenic clot and a
hypercoagulable state in the entire
circulatory system. For coronary
artery thrombi treatment should be
initiated within 4-6 hours from onset
of symptoms.
A. Streptokinase (SK)
B. Urokinase
C. Anisoylated Plasminogen –Streptokinase
Activator Complex ( APSAC)
D. Tissue Plasminogen Activator (t-PA) or
recombinant tissue-type plasminogen
activator ( rt-PA)
E. Retavase
Other Medications: used to reduce
oxygen demand and increase oxygen
supply
Analgesics – Morphine Sulfate
Angiotensin converting enzyme
inhibitor-vasodilation
Beta adrenergic blockers- decrease
contractility & O2 demand; increase
coronary blood flow
Anticoagulants( Heparin, Coumadin)
Calcium channel blockers (Verapamil)
Antidysrhythmic drugs( Lidocaine is
the most common)
Other Medical Interventions:
2.Percutaneous Transluminal Angioplasty (
PTCA)- a non surgical procedure
performed under fluoroscopy, that uses
pressurized balloon catheter to expand
stenotic coronary artery.
3.Intracoronary stents- placement of a
tubular mesh or coilspring device which
is place in the lumen of the coronary
artery.
4.Laser surgery- coronary artery is dilated
with use of laser.
4. Intra-aortic Balloon Pump ( IABP)-
inflation of a balloon in the coronary
artery during diastole and deflated
during sysytole.
5. Coronary Artery Bypass Graft(
CABG)-diversion of blood flow
around an occluded artery. This
conduit is accomplished through
anastomosing of the saphenous
vein or internal mammary artery.
1. Dysrhythmias – due to myocardial
irritability ; Fibrillation is the most
common.
2. Heart Failure.
3. Cardiogenic Shock- due to massive
left ventricular failure.
4. Ventricular aneurysm- a healing
necrotic tissue can cause thinning
and weakening of the
ventricular wall.
5. Pericarditis-an inflammatory
response to myocardial damage.
6. Dressler’s syndrome ( AKA post-
myocardial infarction syndrome)- a
late Pericarditis, with precordial pain,
friction rub, fever, peuritis and/or
pleural effusion.
7. Pulmonary embolism.
8. Interventricular septal rupture.
9. Papillary muscle rupture.
Description: the exchange of oxygen for
carbon dioxide in the lungs is inadequate
for oxygen consumption and carbon
dioxide production within the body’s
cells.

ARDS is characterized by:

Hypoxemia: PO2 below 50mmHg.
Hypercapnia: PCO2 above 45 mmHg.
 ARDS is an unexpected, catastrophic
pulmonary complication occurring in a
person with no previous pulmonary
problems. The mortality rate is high
 Common causes of
respiratory failure include:

3. COPD 1. Emboli
4. Pneumonia 2. Drug overdose
5. Tuberculosis 3. Fluid overload
6. Contusion 4. DIC
7. Aspiration 5. Shock
8. Inhaled toxins
Nursing assessment

• Dyspnea, tachypnea
• Intercoastal retractions
• Cyanosis
• Hypoxemia: PO2< 50 mmHg
with FiO2 > 60%
• Diffuse pulmonary infiltrates
seen on chest x-ray as “white-
out” appearance
• verbalized anxiety; restlessness
(Nursing Diagnoses)

• Impaired gas exchange

• Ineffective airway clearance
• Ineffective breathing pattern
• decreased cardiac output
• Fluid volume excess
 Interventions
• Maintain client on a ventilator with
the correct settings.
• Provide care for either an oral
airway or a tracheostomy. (Suction
ONLY when secretions are present)
• Monitor breath sounds for
pneumothorax especially when
positive end expiratory pressure
(PEEP) is used to keep small airways
open. The amount of pressure can be
set with the ventilator and is usually
around 5-10 cm of water.
• Provide emotional support to
1. Monitor client
hemodynamically with essential
vital signs and cardiac monitor.
2. Monitor ABGs routinely.
3. Monitor vital organ status:
central nervous system, level of
consciousness, renal system
output and myocardium (apical
pulse, blood pressure).
4. Monitor fluid and electrolyte
balance.
ArtificialSurfactant
(Survanta/Beractant) ?
Nitric Oxide –pulmonary vasodilator ?
Dobutamine/Dopamine for fluid
instability
Steroids
Antibiotics
Ventilatory support with PEEP
Baro trauma, VA pneumonia,
pulmonary fibrosis, Pulmonary
embolism
Stress ulcers, GIT hemorrhage
Arrhythmias
ARF
Pneumothorax and tracheal stenosis
Malnutrition and electrolyte inbalance
MOSF – from endothelial damage by
circulating immune complexes
 SHOCK

Description: Widespread,
serious reduction of tissue
perfusion (lack of oxygen and
nutrients), which, if prolonged,
leads to generalized impairment
of cellular functioning.
At risk for developing shock
include:
2.The very young or the very old client
3.Post-MI clients
4.Clients with severe
dysrhythmia
6.Clients with adrenocortical
dysfunction
8.Persons with a history of
recent hemorrhage or
blood loss.
11.Clients with burns
 TYPES OF SHOCK

TYPE DESCRIPTION

HYPOVOLEMI
C Related to external or
internal blood/fluid loss
(most common cause of
CARDIOGENI
C/OBSTRUCTI
shock);
Related hemorrhage, burns, to
VE dehydration
ischemia/impairment in
tissue perfusion from
myocardial infarction, serious
arrhythmia, or congestive
heart failure. All of these
Distributiv Results from inadequate
e
SHOCK
vascular tone.
Blood volume remains
normal
Vascular space increases
dramatically because of
massive vasodilation
1.Neuroge Blocking of the sympathetic
nic
NS in SCI leads to massive
peripheral vasodilation from
an unopposed
parasympathetic NS.
 2. Related to allergens
VASOGENI
C (anaphylaxis), spinal cord
ANAPHYLACT
IC
injury, or peripheral
neuropathies, all resulting in
venous pooling and
decreased blood return to
the heart, which decreases
cardiac output over
3. time.Warm
Related to skin,
endotoxins
SEPTIC bronchoconstriction
released from rashes
bacteria,
may
which be causes
observed with
vascular
products
pooling, of inflammation
diminished venous
 STAGES OF HYPOVOLEMIC SHOCK
STAGE SIGNS AND CLINICAL DESCRIPTION
SYMPTOMS

STAGE I: •Apprehension •Arteriolar

INITIAL and constriction
STAGE restlessness •Increased
Blood loss (first signs of production of ADH
of less shock) •Arterial pressure
than 10%. •Increased is maintained
Compensa heart rate •Cardiac output
tory •Cool, pale usually normal (for
mechanis skin healthy
ms •Fatigue individuals)
triggered. •Selective
reduction of blood
STAGE •Flattened •Marked
II: neck veins reduction in
COMPENSATO and delayed cardiac output
RY STAGE venous filling •Arterial pressure
Bloodvolu time decline (despite
me •Increased compensatory
reduced pulse and arteriolar
by 15 to respirations vasoconstriction)
25%. •Pallor, •Massive
Decompens
diaphoresis adrenergic
ation compensatory
begins. and cool skin
•Decreased response
urinary resulting in:
output tachycardia,
STAGE •Edema •Rapid
III: •Increased circulatory
PROGRESSI blood viscosity deterioration
VE STAGE
•Excessively •Decreased
low blood cardiac output
pressure •Decreased
•Dysrhythmia, tissue perfusion
ischemia and •Reduced blood
MI volume
•Weak,
thready, or
absent
peripheral
STAGE IV: •Profound •Cell destruction
Irreversible
STAGE hypotension, so severe death
unresponsive to is inevitable
vasopressor •Multiple organ
drugs system failure
•Severe
hypoxemia,
unresponsive to
oxygen
administration
•Anuria, renal
shutdown
•Heart rate
slows, BP falls,
Nursing Assessment

Vital Signs:
4.Tachycardia (>100 bpm)
5.Tachypnea (>24 cpm)
6.Blood pressure decreased
(systolic <80 mmHg)
Mental Status Exam:
9.Early shock: restless, hyper-alert
10.Late shock: decreased alertness,
lethargy, coma
Skin Changes:
2.Cool, clammy (warm skin in vasogenic
and early shock)
3.Diaphoresis
4.Pale
Fluid Status (acute tubular necrosis
can happen quickly in shock):
• Urine output decreases or an
imbalance between intake and output
occurs
• Abnormal CVP (>4 cm of H2O).
• Urine specific gravity >1.020
(Nursing Diagnosis)

3. Fluid volume deficit

4. Decreased cardiac
output

6. Altered thought
process

7. Anxiety (family and

individual)
Monitor arterial pressure by
understanding the concepts
related to arterial pressure
Monitor vital signs and
arrhythmias every 15 minutes
or more often depending on the
stability of the client.
Assess urine every hour to
maintain at least 30 ml/hr.
Notify healthcare provider if
urine output drops below 30
Administer fluids as prescribed by
provider: blood, colloids, or
electrolyte solutions until
designated CVP is reached. (In
shock, the healthcare provider
often orders fluids to elevate CVP
16-19 cm of H2O as compensation
for decreased cardiac output).
Place client in modified
Trendelenburg’s position (feet up
30-45 degrees, head flat).
Administer medications IV (not IM
or subQ) until perfusion improves in
HINT: If cardiogenic shock exists
with the presence of pulmonary
edema, i.e. from pump failure,
position client to REDUCE venous
return (high-Fowler’s with legs
down) in order to decrease venous
return further to the left ventricle.
Keep client warm (increase heat in
room or put warm blankets in client,
but not too hot).
Keep side rails up during all
procedures (clients in shock
experience mental confusion and may
easily be injured by falls).
Obtain blood for laboratory work
as prescribed: CBC, electrolytes,
BUN, creatinine (renal damage),
and blood gases
(oxygenation).
Drugs of choice for shock:
2. Digitalis preparations:
increase contractility of the
heart muscle
3. Vasoconstrictors
( Dopamine): generalized
vasoconstriction to provide
more available blood to the
heart to help maintain
cardiac output.
Vasodilators – for blood supply to
important organs and in cardiogenic
shock
Steroids
Heparin
Naloxone- reverses the effects of
hypotension as an opiate antagonist
Epinephrine- for anaphylactic shock
H2 receptor antagonists – ulcers
Opioids – for cardiogenic shock
Calcium gluconate- for blood clotting
and muscular function
Blood- whole ( to replace large
volume loss), packed RBC 9 for
moderate blood loss bec they
replenish RBC and improve oxygen –
carrying capacity without adding
excessive volume), autotransfusion
(trauma). As a rule of thumb, Hct.
Rises about 4% and Hgb rises about
1 g % for each unit of packed RBC
administered.
Fluid replacement- Crystalloids ( for
F/E replacement) ,Colloids( plasma
protein fraction, fresh-frozen plasma,
albumin, dextran, hetasarch ( plasma
expander) are used to restore plasma
volume and colloidal osmotic
pressure bec. they contain large
molecules usually proteins or
starches)
•Isotonic solutions:
•Normal saline (0.9% NS)
•Lactated Ringers (LR)
•5% dextrose in water (D5W is on the
low end of isotonic-some sources
classify as hypotonic)
Hypotonic solutions:
6.0.3 % NaCl
7.0.45 NS
8.D 2.5 in H20
•Hypertonic saline solutions are available
but used only when serum osmolality is
dangerously low
•5% dextrose in LR (D5LR)
•5% dextrose in 0.45% saline (D5 ½ NS)
•5% dextrose in 0.9% saline (D5NS)
Description: a coagulation
disorder with paradoxical
thrombus and hemorrhage. DIC is
an acute complication of
conditions such as hypotension
and septicemia, suspected when
there is bloody oozing from two
or more unexpected sites. The
first phase involves abnormal
clotting factors, and results in an
The diagnosis is based on
laboratory findings:
2. Prolonged PT
3. Prolonged PTT
4. Decreased fibrinogen
5. Decreased platelet count
6. Increased Fibrin Degradation
(split) Products (FDP)
Nursing Assessment
Petechiae, purpura, hematomas
Oozing from IV sites, drains, gums
and wounds
GI and GU bleeding
Hemoptysis
Hypotension, tachycardia
Pain

Nursing Diagnoses
10. Potential for injury
11. Alteration in tissue perfusion
Nursing Plans and Interventions
2. Monitor client for bleeding.
3. Monitor vital signs.
4. Protect client from injury and bleeding:
• Provide gentle oral care with mouth
swabs
• Minimize needle sticks, use smallest
gauge needle possible.
• Turn frequently to eliminate pressure
points.
• Minimize number of blood pressures
taken by cuff.
4. Administer Heparin IV
during the first phase to
inhibit
coagulation.
5. If in hemorrhagic phase,
administer clotting factors

6. Provide emotional support

to decrease anxiety.
Description: dilation of the abdominal
aorta caused by an alteration in the
integrity of its wall.

Most common cause of AAA is

atherosclerosis
It can also be a late manifestation of
syphilis
Without treatment, rupture and death
will occur
It is often asymptomatic
Most common symptom is abdominal
pain or low back pain with the
Nursing Assessment
2. Bruit (swooshing sound heard over
a constricted artery when
auscultated) heard over abdominal
aorta, pulsation in upper abdomen.
3. Abdominal or lower back pain.
4. Abdominal x-ray will confirm
diagnosis if aneurysm is calcified
(aortagram, angiogram, abdominal
ultrasound).
5. Symptoms of rupture: hypovolemic
or cardiogenic shock with sudden,
Nursing Diagnosis
2. Activity intolerance
3. Impaired skin integrity
4. Anxiety
Nursing Plans and
Interventions
3. Assess all peripheral pulses and
vital signs regularly
4. Observe for signs of occlusion
after graft
5. Observe renal functioning for
signs of kidney damage (artery
clamped during surgery may
result in kidney damage).
MOSF= Multiple Organ System Failure
Multiple Organ Dysfunction Syndrome
( MODS)
a syndrome that occurs when one or more
than one system/organ cannot support its
activities.
 Factors Influencing the development of
MODS: Gram negative sepsis ( #1 risk),
immunosuppressants, traumatic injury,
sleep deprivation, malnutrition, blood
transfusions, age over 65.
 Pathophysiology: the 3 Is of MODS are:
persistent Inflammation,
Infection (sepsis),
Ischemia.
 The precursor of MODS is systemic
inflammatory response syndrome ( SIRS)

3. Stimulation of the inflammatory-immune

response ( IIR) which
4. Sympathetic nervous system stimulation
and release of catecholamines
5. Endothelial damage and embolus
formation. Complement activation occurs
GOAL: is to induce inflammation, the
goal of inflammation is to protect the
body, limit injury extent , and
promote healing at the damaged site)
Other Mediators involved in the IIR
are WBC, platelet, T cells, B cells, and
histamine.
Altered perfusion r/t to small
microvasculature emboli and
respiratory insufficiency causes
shunting of blood to major organs
until compensatory mechanisms fail.
The organs affected are usually the
lungs, liver kidney, heart and brain.
Modified APACHE II Criteria for
Diagnosing Multiple Organ System
Failure ( Black and Jacobs, 1997)
I. Cardiovascular Failure ( presence of one or
more of the ff)
 HR less than 54 beats / min
 Mean arterial pressure equal or less that
49 mm Hg (systolic pressure of equal or
less than 60mmHg)
 Occurrence of Ventricular Tachycardia/
Fibrillation
 Serum pH of equal or less than 7.24 with a
PaCo2 of equal or less than 40 mmHg
II. Respiratory Failure ( presence of one or
more of the following)

 RR of less than or equal to 5/min. equal to

or greater than 49/min, PaCO2 equal or
greater than 50mmHg
 Alveolar Arterial Oxygen difference equal
or greater then 350mmHg calculated as
follows: (713 x % Oxygen in inspired gas)-
PaCO2- PaO2
 Dependent on ventilator on the 2nd day
III. Renal Failure ( presence of one or
more of the ff)
*Urine output equal or less than 479
ml/24 hrs. or equal or less than
159ml/8 hrs.
* Serum BUN equal to or greater than
100mg/dl
* Serum Creatinine equal to or
greater than 3.5 mg/dl
IV. Hematologic Failure ( presence of
one or more of the ff)

*WBC equal or less than 1000/ul

( Normal is 4,000 to 10,000/ ul)
*Platelet equal or less than 20,000
/mm3
* Hematocrit equal or less than 20%
V. Neurologic Failure
Glasgow coma score equal or < than
6 ( in the absence of sedation )

VI. Hepatic Failure

Serum Bilirubin equal or greater than
6 mg/dl
Prothrombin Time equal to or greater
than 4 sec over control in the
absence of systemic anticoagulation
Assessment:

 Early: Vasodilation and ↓ PR With normal

BP, Cardiac output increases to maintain
blood pressure= initial hyperthermia ( skin
warm, pink, and dry with shaking chills
although the reverse may occur in the
elderly) ,
 Increase renal blood flow ( polyuria),
 Hyperventilation (Causes resp alkalosis),
 Signs of tissue hypoxia manifest due to
oxyhemoglobin dissociation ; Hemoglobin
is reluctant to release oxygen to cells.
 Late: Hypotension due decreased
cardiac output ( PR is ↑ via
catecholamine release due to
sympathetic nervous system
stimulation) ;
 Pulse becomes weak and thready; ST
and T wave changes on ECG ( due to ↓
myocardial perfusion);
 Cold, moist, pale skin, mottling and
cyanosis, hematologic changes( DIC or
primary bleeding problem),
 Hypoxia (↑HR,↑RR, restlessness,
diaphoresis, lethargy, confusion, and
pallor) and
 ↓perfusion evident
 metabolic acidosis develops.
Others:
Glucose: initially increased,
gluconeogenesis occurs leading
to lactic acidiosis; protein
catabolism causes negative
nitrogen balance and proteinuria
Generalized acidotic state and
decreased cellular energy cause
cell death and organ failure
Mortality is up to 90%
Management:

 Monitor V/S, Neuro status, Measure

I/O, Bowel sounds/ Abdominal
distention, Abdominal girth, Occult
blood
Ventilatory support, ABG monitoring,
pulse oximetry
Maintain + nitrogen balance ( enteral
feeding)
MEDICATIONS :
 antibiotics, antacids, histamine
antagonists, analgesics, anti-anxiety
agents, sedate as ordered to ↓
metabolic needs, anti-inflammatories,
vasoactive agents, inotropes, fluids ,
steroids ( not proven to be beneficial)
FUTURE TRENDS in therapy:
Cyclosporine vs. FK-586;
monoclonal/polyclonal antibodies.
 Sample Questions
Which of the following nursing
orders would be found on the
care plan for a client for the first
24 hours after an MI?
A. Utilize bedside commode for
bowel movements
B. 200 calorie soft diet
C. Feed the patient
D. Administer promethazine daily
Which of the following would be
included in the discharge plan
for a client after MI?
A. Don’t begin sexual intercourse
until after 3 months
B. Begin walking frequently
C. Take one aspirin every 8 hours
as ordered
D. Continue previous lifestyle
when ready
To prevent the leaking of blood into
surrounding tissue following blood
extraction for ABG determination,
the nurse should implement which
nursing measure:
A. Apply ice to the puncture site
B. Maintain manual compression
over the puncture site for at least
one minute
C. Elevate the limb on several
pillows
The client is an asthmatic and in acute
respiratory distress. The nurse
auscultates the lungs and notes no
inspiratory wheezing. What should
this finding suggest to the nurse?
A. Airway constriction requiring
intensive interventions
B. An appropriate reaction to the
medications used in the
management of the client
C. The need to assess the client
further for signs of pleural
effusion
D. Overuse of the intercostal