CRITICAL CARE NURSING

CHAPTER 1: LEGAL ETHICAL ISSUES

A. Documentation
B. Informed consent
C. Declaring death
D. Patients rights
E. DNR orders
F. Advance directives
G. Goal Samaritan act
H. Legal process
I. Ethical principles
a. Patient autonomy
b. Justice
c. Veracity
d. Fidelity
e. Beneficence
f. Non-maleficence

CHAPTER II: ACUTE CORONARY SYNDROME
A. ACS vs AMI
B. Etiology and pathophysiology
C. Triad of diagnosis
a. Clinical presentation/ manifestation
b. ECG
c. Cardiac biomarkers
D. Management and therapy ( American Health
Association Algorithm)

CHAPTER III: ARF
A. Differentiation of ARF and ARDS
B. Etiology and pathophysiology
C. Clinical manifestations and differential
diagnosis
D. Medical management and therapy
a. Respiratory therapy
b. Pharmacological approach
c. Medical supportive therapy

CHAPTER IV: ACUTE KIDNEY INJURY
A. Etiology and pathophysiology
a. Pre-renal failure
b. Renal failure
c. Post-renal failure
B. Clinical manifestation with diagnostic studies
C. Medical management and therapy
a. Dialysis
b. Drug therapy
D. Management of ABG abnormality
E. Management of electrolyte problems
CHAPTER V: SHOCK
A. Etiology/ classification
a. Hypovolemic
b. Cardiogenic shock
c. Septic shock
d. Neurogenic shock
e. Anaphylactic
B. Clinical manifestation with diagnostic studies
C. Differential diagnosis/ category
a. Hypovolemic
b. Cardiogenic
c. Obstructive
d. Distributive
D. Medical management and therapy

CHAPTER VI: MULTIORGAN DYSFUNCTION/
FAILURE












































CHAPTER I: LEGAL ETHICAL ISSUES

A. DOCUMENTATION
Whole chart

PURPOSE:
1. Communication among health care
providers
2. To plan and evaluate nursing care
3. To demonstrate use of nursing process
4. To show progress of patient care
5. To protect patient
6. To protect health care providers
7. To reflect nursing observation, intervention
and evaluation
8. To inform consent based on the autonomy
of individuals

B. INFORMED CONSENT
Mental capacity
Legal age
All procedures should be explained by
the physician

Special consideration for minors:
a. Abandoned
b. Self-supporting
c. Already married
d. Degree holder

Implied consent
Emergency cases
Even without consent

C. DECLARING DEATH
Responsibility of the physician

Brain Death
Irreversible cessation of the activity in
the central nervous system

D. DO NOT RESCUCITATE ORDERS
Significant others will sign the consent
Effective only for 24 hours
Once discharged: not effective
Legal age, mentally capable and
informed

Form contains:
a. Stop mechanical ventilator
b. CPR
c. Emergency medications

E. ADVANCE DERICTIVES
Signed by the patient

F. GOOD SAMARITAN ACT
Provides immunity from civil liability

G. LEGAL PROCESS

Negligence
An unintentional act on the failure to
do what is reasonable

H. ETHICAL PRINCIPLES

1. Fidelity
Keeping professional obligations as
professional nurses

2. Patients autonomy
Self determination
Freedom of choice

3. Justice
Right vs. wrong
Discrimination

4. Veracity
Telling the truth
Honesty and integrity
Right to information

5. Beneficence
Bring good

6. Non-maleficence
Do no harm

I. PATIENTS RIGHTS

1. Right to refuse treatment
Refusal of care by a competent
adult

2. Right to information
Right to informed consent

3. Right to confidentiality
Right of client for anonymity




MYRA LEVINES CONSERVATION THEORY

1) CONSERVATION OF ENERGY
Refers to balancing energy input
and output to avoid excessive
fatigue
Includes adequate rest, nutrition,
exercises
Ex: availability of adequate rest,
maintenance of adequate nutrition

2) CONSERVATION OF STRUCTURAL
INTEGRITY
Refers to maintaining or restoring the
structure of the body preventing
physical breakdown and promoting
healing
Ex: assist patient in ROM exercises
Maintenance of patients personal
hygiene

3) CONSERVATION OF PERSONAL
INTEGRITY
Intrinsic
Recognizes the individual as one who
strives for recognition
Ex: recognize and respect patients
space needs

4) CONSERVATION OF SOCIAL INTEGRITY
Extrinsic
An individual is recognized as someone
who resides within a family, a
community, a religious group, a
political system and a nation
Ex: help the individual to perceive his/
her place in a family, community and
society

MADELEINE LEININGERS TRANSCULTURAL
THEORY
CULTURAL THEORY OF DIVERSITY
Bridging patient culture versus nursing care

CULTURE CARE:
a. Preservation/ maintenance
b. Accommodation / negotiation
c. Re-patterning/ restructuring

FLORENCE NIGHTINGALES ENVIRONMENTAL
MODEL
a. Home
b. Ventilation and warming
c. Light
d. Noise
e. Variety
f. Bed and bedding
g. Cleaning of rooms and walls

JEAN WATSONS TRANSPERSONAL CARING
Caring can be practiced and demonstrated

10 CARRATIVE FACTORS OR CARITAS PROCESS
1. Formation of a Humanistic Altruistic System
of Values
2. Instillation of Faith-Hope
3. Cultivation of Sensitivity to Self and Others
4. Development of a Helping-Trust Relationship
5. Promotion and Acceptance of the Expression
of Positive and Negative Feelings
6. Systematic Use of the Scientific Problem-
SolvingMethod for Decision Making
7. Promotion of Interpersonal Teaching-Learning
8. Provision for a Supportive, Protective, and
Corrective Mental, Physical, Sociocultural, and
spiritual environment
9. Assistance with Gratification of Human Needs
10. Allowance for Existential-Phenomenological
Forces

BETTY NEUMANS SYSTEM MODEL

A. BASIC STRUCTURE
o Main survival of patient
o The core structure consists of basic
survival factors
o Genetic factors or innate

B. LINE OF RESISTANCE
o Help defend against stressors
o It can be depleted or expanded
o Bodys immune system
o Coping mechanism

C. NORMAL LINE OF DEFENSE
o Represents a stability state
o Coping patterns, lifestyle,
developmental stage, age

D. FLEXIBLE LINE OF DEFENSE
o Dynamic and can be rapidly altered
over a short time
o Perceived as protective buffer for
preventing stressors from breaking
through usual wellness state
o Preserve wellness
o Sleep/ rest

STRESSORS PENETRATE THE CORE:
a. Interpersonal
o Autoimmune response
b. Intrapersonal
o Role expectations
c. Extra personal
o Social policy

PREVENTIONS:
A. PRIMARY PREVENTION
Nothing happened yet
Facilitates protection of core
FLEXIBLE LINE OF DEFENSE
Stress management
Relaxation techniques
Anger management
Smoking cessation

B. SECONDARY PREVENTION
Treat symptoms
NORMAL LINE OF DEFENSE
Medication
Opportunity to verbalize feelings and
concerns

C. TERTIARY PREVENTION
Towards rehabilitation
Check up with psychologist
Maintaining support system

Depends on the reaction person (
pessimistic vs. optimistic)
Reconstitution reinstate wellness

IDA JEAN ORLANDOS NURSING PROCESS
DISCIPLINE

Need

Presenting behavior of a patient( subjective or
objective assessment)

Automatic nursing action

Derivative nursing action (with nursing theory)

Nursing Process discipline
(Dynamic approach)

Patients need resolved


1. SELF CARE AGENCY
SELF CARE AGENT- patient
DEPENDENT CARE AGENT

2. SELF CARE DEMAND
UNIVERSAL common to all
DEVELOPMENTAL needs resulting
from maturation
HEALTH DEVIATION from illness,
injury

3. NURSING AGENCY
WHOLLY COMPENSATORY very
dependent
PARTIALLY assistance in some
SUPPORTIVE EDUCATIVE needs
help on decision-making, behavioral
control, acquisition of knowledge

DOROTHY JOHNSONS BEHAVIORAL
SYSTEM MODEL

PERSON- a behavioral system
BEHAVIOR a repetitive purposeful
predictable actions

When 1 is dysfunctional : patient is ill

7 SUBSYSTEMS
1. AFFILIATIVE SUBSYSTEM
Social bonds
2. ACHIEVEMENT
Efforts to gain mastery and
control
3. AGGRESSIVE
Self- protection and preservation
4. DEPENDENCY
Helping or nurturing
5. SEXUAL
Procreation and gratification
6. INGESTION
Food intake
7. ELIMINATIVE
Excretion

LYDIA HALLS CARE, CORE AND CURE


SR. CALISTA ROYS ADAPTATION THEORY

ADAPT

4 MODES

1. Physiologic
2. Self-concept
3. Role function
4. Interdependence





ACUTE CORONARY SYNDROME
obstruction/ occlusion of coronaries -->
interruption of blood flow and oxygen in
myocardial tissues
collective term: requires broad clinical
manifestation which is correlated to main
problem ( dec. coronary blood flow)

COLLECTIVE TERM

CAD
Atherosclerosis: lipids on intimal and medial
lining of the blood vessel
Arteriosclerosis: hardening of arteries

Plaque formation (ATHEROMA)

Occlusion

Increase vascular resistance

insufficient blood and oxygen supply

chest pain

UNSTABLE ANGINA
dec. oxygen supply
paroxysm of pain usually at rest known as
PREINFARCTION ANGINA

MYOCARDIAL INFACTION
causes damage of myocardial tissue->necrosis

RISK FACTORS OF OF CAD (SAFE SEX)
S-smoking: 1-2 packs per day(chronic)
A- age: old(geriatrics 65 y/o and above)
new(30-50 y/o)
-diet, lifestyle
F- family history of CAD
E- elevated cholesterol/ uric acid
SEX : males and post menopausal women

ANGINAL PECTORIS
HISTORY ASSESSMENT:
Precipitating Factors: 4E's
E- exertion - strenuous physical activity
E- extreme temperature - too hot / cold
E- eating - heavy meal
E- emotion: excitement, sexual activity

TYPES OF ANGINA:(SUVIS)
S- stable: caused by exertion
U- unstable/ Preinfaction angina: present
at rest
V- variant/ Prinzmetals/ Nocturnal: at
night/rest
I- intractable: severe case of angina that
does not respond to treatment and
management
S- silent: asymptomatic

TREATMENT:
Nitroglycerides- 3 doses max at 5 mins
interval (remove previous and place new on
the other side)

MYOCARDIAL INFACTION
presence of necrosis

TRIAD OF DIAGNOSTICS

1. CLINICAL PRESENTATION
GOAL: assess severity
chest pain

PATHO:
Atherosclerosis

atheroma

dec. blood supply

dec oxygen

MI

anaerobic myocardial metabolism

lactic acid

chest pain

location
characteristics:RETROSTERNAL HEAVINESS
/ CRASHING AND SQUIZING
duration: >30 mins
radiates: shoulder, neck, left arm, back
accompanied by: DANCEPAD
Dyspnea/ DOB
Anxiety
Nausea and vomiting
Cold, clammy skin
Elevated temperature/ epigastric pain
Pallor
AM : early in the morning
Diaphoresis
2. ECG ANALYSIS

MAIN PROBLEM (3 I's) IMPLICATIONS (3D's) ECG RESULT ANALYSIS
Ischemia Decreased oxygen
supply

T wave inversion
Injury Destruction of
myocardial tissue

ST segment
elevation

Infarction Death of
myocardial tissue

(+) pathologic Q
wave


3. CARDIAC BIOMARKERS
CARDIAC BIOMARKER NORMAL VALUES IMPLICATIONS NURSING
CONSIDERATIONS
a. CK-MB
creatinine kinase
M: 5-55 U/L
F: 5-25 U/L
Increased in MI
within 4 hours
avoid vigorous
activity
no IM injection
before test
b. LDH
lactic
dehydrogenase
70-200 IU/L flipped LDH
Normally: LDH1>LDH2
In MI: LDH2>LDH1
no specific nursing
consideration
c. Myoglobin <100mg/dl increased in MI
within 1-3 hours
increased result
may be related to
muscular or renal
disease
not single
confirmatory
d. TROP I
TROP T
< 0.6 mg/dl
0-0.2 mg/dl
Increased within
3-4 hours
no IM injections
e. LIPID PROFILE
serum lipids
cholesterol
triglyceride
LDL
HDL
NPO post
midnight
(12hours) ideally

MANAGEMENT of CHEST PAIN: MONA
Morphine Sulfate
Oxygen supplementation (1-2Lpm)
Nitroglycerine
Aspirin (160-300 doses)

1. Oxygen
2. Rapid triage + 12 lead ECG
3. Iv access
4. Blood sample extraction ( DONE NOT <10
MINS)

12 LEAD ECG TWO RESULTS

a. ST depression with T wave inversion
Awaits cardiac biomarkers

b. ST elevation

Reperfusion therapy

1. DOOR TO NEEDLE (<30mins)
Medications
Thrombolytics
Eg. Streptokinase

2. DOOR TO BALLOON(<90 mins)
PTCA and CABG
Percutaneous Transluminal Coronary
Angioplasty
Coronary Artery Bypass Grafting

MEDICATIONS:
1. Aspirin: platelet aggregation inhibitor
2. Anticoagulant medicines: Heparin
3. Antihypertensive drugs
4. Nitrates : reduces oxygen requirement of the
heart muscle

NURSING INTERVENTIONS:

1. Monitor and improve patients
cardiopulmonary state
Monitor ECG
Monitor urine output
Report <30ml/ hr

2. Monitor for complications
Dysrhythmias
Within 1 hour may have Ventricular
Tachycardia

3. Minimize client anxiety
Proper dessimination of information
4. Minimize metabolic demands
Soft diet: dec. sodium, salt and
unsaturated fats

5. Provide oxygen (2lpm)
6. Bedrest
Semifowlers

7. Sexual activity
Refer to cardiologist
3 flight of stairs assessment

8. Health teaching
Avoid foods rich in vitamin K
Eg. Green leafy vegetables, spinach
Report bleeding


PHARMACOLOGIC THERAPY
The patient with an acute MI receives the same
medications as the patient with unstable angina, with
the possible additions of thrombolytics, analgesics,
and angiotensin-converting enzyme (ACE) inhibitors.
Patients should receive a beta-blocker initially,
throughout the hospitalization, and a prescription to
continue its use after hospital discharge.

Thrombolytics. Thrombolytics are medications that
are usually administered intravenously, although
some may also be given directly into the coronary
artery in the cardiac catheterization laboratory (Chart
28-7). The purpose of thrombolytics is to dissolve
and lyse the thrombus in a coronary artery
(thrombolysis), allowing blood to flow through the
coronary artery again (reperfusion), minimizing the
size of the infarction, and preserving ventricular
function.
Even though thrombolytics may dissolve the
thrombus, they do not affect the underlying
atherosclerotic lesion. The patient may be referred
for a cardiac catheterization and other invasive
interventions.

To be effective, thrombolytics must be administered
as early as possible after the onset of symptoms that
indicate an acute MI. They are not given to patients
with unstable angina. Hospitals monitor their ability
to administer these medications within 30 minutes
from the time the patient arrives in the emergency
department. This is called door-to-needle time (Ryan
et al., 1999). The thrombolytic agents used most
often are streptokinase (Kabikinase, Streptase),
alteplase (Activase), and reteplase (r-PA, TNKase).
Anistreplase (Eminase) is another thrombolytic agent
that may be used.

Streptokinase increases the amount of plasminogen
activator, which then increases the amount of
circulating and clot-bound plasmin. Because
streptokinase is made from a bacterium, its use also
entails a risk of an allergic reaction. Vasculitis has
occurred up to 9 days after administration.
Streptokinase is not used if the patient has been
exposed to a recent Streptococcus infection or has
received streptokinase in the past 6 to 12 months.
Alteplase is a type of tissue plasminogen activator (t-
PA). In contrast to streptokinase, alteplase activates
the plasminogen on the clot more than the circulating
plasminogen. Because it does not decrease the
clotting factors as much as streptokinase,
unfractionated or low molecular weight heparin is
used with t-PA to prevent another clot from forming
at the same lesion site. Because t-PA is a naturally
occurring enzyme, allergic reactions are minimized,
but t-PA costs considerably more than streptokinase.
Reteplase is structurally very similar to alteplase and
has similar effects. Anistreplase is similar to
streptokinase and has similar effects.

Analgesics. The analgesic of choice for acute MI is
morphine sulfate (Duramorph, Astramorph)
administered in intravenous boluses. Morphine
reduces pain and anxiety. It reduces preload, which
decreases the workload of the heart. Morphine also
relaxes bronchioles to enhance oxygenation. The
cardiovascular response to morphine is monitored
carefully, particularly the blood pressure, which can
be lowered, and the respiratory rate, which can be
depressed. Because morphine decreases sensation of
pain, STsegment monitoring may be a better
indicator of subsequent ischemia than assessment of
pain.

Angiotensin-Converting Enzyme Inhibitors
(ACE-I).
Angiotensin I is formed when the kidneys release
renin in response to decreased blood flow.
Angiotensin I is converted to angiotensin II by ACE, a
substance found in the lumen of all blood vessels,
especially the pulmonary vasculature. Angiotensin II
causes the blood vessels to constrict and the kidneys
to retain sodium and fluid while excreting potassium.
These actions increase circulating fluid and raise the
pressure against which the heart must pump,
resulting in significantly increased cardiac workload.
ACE inhibitors

(ACE-I) prevent the conversion of angiotensin from I
to II. In the absence of angiotensin II, the blood
pressure decreases and the kidneys excrete sodium
and fluid (diuresis), decreasing the oxygen demand
of the heart. Use of ACE inhibitors in patients after
MI decreases the mortality rate and prevents the
onset of heart failure. It is important to ensure that
the patient is not hypotensive, hyponatremic,
hypovolemic, or hyperkalemic before ACE-I
administration. Blood pressure, urine output, and
serum sodium, potassium, and creatinine levels need
to be monitored closely.