Medical-Surgical Nursing

(Stress, Inflammation and Pain)

Dynamic Balance: Steady Balance

• Claude Bernard: “Fixity of internal milieu”

• Walter Cannon: “ Homeostasis”

• Rene Jules Dubos: “Homeostasis and Adaptation”

o Homeostasis- stead state within the body.

Stress and Adaptation

Stress

• A disruptive condition that occurs in response to adverse

influences from the internal or external environments.

• It is a state produced by a change in the environment that is

perceived as challenging, threatening, or damaging to a
person’s dynamic balance or equilibrium.

Adaptation

• It is a constant, ongoing process that requires change in

structure, function, or behavior so that a person is better
suited to the environment.

• A change or alteration designed to assist in adapting to a

new situation or environment.

Types of Stressors

• Physical Stressors- cold, heat, chemical agents.

• Biological/ Physiological- pain and fatigue.

• Psychosocial- fear of failing exams, loss of job and waiting

for the result of a diagnostic exam.

• Day to day frustration/hassles- caught in traffic jam,

experiencing computer down time, having argument with a
roommate/spouse.

• Major complex occurrence involving large group- terrorism,

war

• Stressors that occur less frequently and involving fewer

people- death, birth, marriage, divorce and retirement.
 • Acute, time-limited stressors- studying foe final exam.

• Stressor sequence- series of stressful events

• Chronic intermittent stressors- daily hassles.

• Chronic enduring stressors that persistent over time- chronic

illness, disability, poverty.

Psychological Response to Stress (LAZARUS)

• Appraisal of the Stressful Event

o Cognitive appraisal- is a process by which an event is

evaluated with respect to what is at stake (primary
appraisal) and what might and can be done (secondary
appraisal).

o Primary Appraisal- results in the situation being

identified as either nonstressful or stressful.

o Secondary Appraisal- is an evaluation of what might

and can be done about the situation.

o Reappraisal- a change of opinion based on new

information, also occurs.

• Coping With the Stressful Event

o Emotion Focus Coping- seeks t make the person fell

better by lessening the emotional distress.

o Problem-focus coping- aims to make direct changes in

the environment so that the situation can be managed
more effectively.

Physiologic Response to Stress

• Selye’s Theory of Adaptation

o General Adaptation Syndrome

 Alarm- is defensive and anti-inflammatory but self-

limiting
  Resistance- adaptation to the noxious stressor
occurs, and cortisol activity is still increased.

 Exhaustion- endocrine activity increases and this

has negative effects on the body systems that can
lead to death.

o Local Adaptation Syndrome

 Inflammatory Response and repair.

Sympathetic-Adrenal-Medullary Response to Stress

Effects Purpose Mechanism

Increased heart Better perfusion of Increased cardiac
rate and blood vital organs output due to
pressure increased
myocardial
contractility and
heart rate; increased
venous return.
Increased blood Increased available Increased liver and
glucose level energy muscle glycogen
breakdown;
increased
breakdown of
adipose tissue
triglycerides
Mental Acuity Alert state Increased amount of
blood shunted to the
brain from the
abdominal viscera
and skin.
Dilated pupils Increased awareness Contraction of radial
muscle of iris
Increased tension Preparedness for Excitation of muscle;
of skeletal activity, decreased increase in amount
muscles fatigue of blood shunted to
the muscle from the
abdominal viscera
and skin.
Increased Provision of oxygen Stimulation of
ventilation for energy respiratory center in
the medulla;
bronchodilation.
Increased Prevention of Vasoconstriction of
coagulability of hemorrhage in event surface vessels
blood of trauma

• Maladaptive Response to Stress

o Maladaptive- ineffective response to stress.

• Cellular adaptation

• Cells

o Complex units that dynamically respond to the

changing demand and stress of daily life

o Possess a maintenance function and a specialized

function

o Can adapt to environmental stress through structural

and functional changes

o Examples of adaptation

 Hypertrophy, atrophy, hyperplasia, dysplasia,

metaplasia

 Reflect changes in the normal cells in response to

stress

• Maintenance function

o Activities that the cell must perform with respect to

itself

• Specialized function
 o The cell performs in relation to the tissues and organs
of which it is a part

• Hypertrophy and atrophy

o Lead to the changes in the size of cells

• Compensatory hypertrophy

o Result of an enlarged muscle mass

o Commonly occurs in skeletal and cardiac muscle that

experiences a prolonged, increased workload

• Hypertrophy

o Increase in the size leading to the increase in organ size

o Stimulus: increase workload

o Example

 Leg muscles of runner

 Arm muscles in tennis player

 Cardiac muscle in person with hypertension

• Atrophy

o Can be the consequence of:

a. Disease

b. Decreased use

c. Decreased blood supply

d. Loss of nerve supply

e. Inadequate nutrition

o Cell size and organ size decreased

o Structure principally affected:

 a. Skeletal muscle

b. Secondary sex organs

c. Heart

d. Brain

o Shrinkage in size of cells leading to decrease in organ

size

o Stimulus: decrease in

a. Use

b. Blood supply

c. Nutrition

d. Hormonal stimulation

e. Innervation

o Example

 Secondary sex organs in aging person

 Extremity immobilized in cast

• Disuse of a body parts

o Often associated with the aging process and

immobilization

• Hyperplasia

o Increase in the number of new cells in an organ or

tissue

o Tissue mass enlarges

 Cells multiply

 Subjected to increased stimulation

  Reversible when stimulus is removed

o May be hormonally induced

 Increased size of the thyroid gland caused by thyroid

– stimulating hormone

o Increase in number of new cells

o Increase in mitosis

o Stimulus: hormonal influence

o Example

 Breast changes of girl in puberty or of a pregnant

woman

 Regeneration of liver cells

 New blood cells in blood loss

• Neoplasia

o Malignant growth

o Continues growing of cells even though stimulus is

removed

• Dysplasia

o The change in the appearance of cells after they have

been subjected to chronic irritation

o Dysplastic cells

 Have the tendency to become malignant

 o Seen commonly in epithelial cells in the bronchi of
smokers

o Stimulus: reproduction of cells with resulting alteration

of their size and shape

o Example

 Alterations ins epithelial cells of the skin or cervix,

producing irregular tissue changes that could be the
precursors of malignancy

• Metaplasia

o Cell transformation in which highly specialized cells

change to less specialized cells

o Serves as a protective function

o Less specialized cells

 More resistant to stress that stimulated the change

o Example

 Ciliated columnar epithelium lining the bronchi of

smokers is replaced by squamous epithelium (can
survive)

o Transformation of one adult cell type to another

o Stimulus: stress applied to highly specialized cells

o Example

 Changes in the epithelial cells lining bronchi in

response to smoke irritation
• Cellular injury

• Injury

o Disorder in steady state regulation

o Can be caused by stressor that alters the ability of the

cells or system to maintain optimal balance of its
adjustment processes

o Structural or functional changes occur (reversible:

permits recovery; irreversible: leading to disability or
death)

o Steady state regulation is lost

o Changes in function ensure

• Cause of disorder and injury in the system

o May arise from the internal and external environment

o Hypoxia, nutritional imbalance, physical, chemical and

infectious agents, immune mechanisms, genetic
defects, psychogenic factor

• Most common cause

a. Hypoxia

b. Chemical injury

c. Infectious agents

• Agents act at the cellular level by damaging or destroying:

a. Integrity of the cell membrane (necessary for ionic

balance)

b. The ability of the cell to transform energy

c. The ability of the cell to synthesize enzymes and other

necessary proteins.

d. The ability of the cell to grow and reproduce.

• Homeostatic adjustments

o Concerned with the small changes within the body’s

systems

• Adaptive changes

o Compensation occurs

o Steady state is achieved (may be a new level)

• Hypoxia

o Inadequate cellular oxygenation

o Causes:

 Decrease in blood supply in the area

 Decrease blood carrying capacity of the blood

 Ventilation/perfusion or respiratory problem that

reduces the amount of oxygen available in the
blood.

 Problem in the cell’s enzyme system that makes it

unable to use the oxygen delivered to it.

 Common cause: ischemia.

• Nutritional Imbalance

o It refers to a relative or absolute deficiency or excess of

one or more essential nutrients.

• Physical Agents

o Temperature

o Radiation and electrical shock

o Mechanical trauma

• Chemical Agents

o Poison, drugs, alcohol.

 • Infectious Agents

o Viruses, bacteria, fungi, protozoan.

• Disordered Immune Response

• Genetic Disorder

Inflammation

• Inflammation- is a defensive reaction intended to neutralize,

control, or eliminate the offending agent and to prepare the
site for repair.

• Types of Inflammation

o Acute Inflammation- is characterized by local vascular

and exudative changes and usually lasts less than 2
weeks.

o Chronic Inflammation- develops if the injurious agent

persists and the acute response is perpetuated.

o Subacute Inflammation- falls between acute and

chronic inflammation.

• Cellular Healing

o Regeneration

o Replacement

 Primary Intension Healing- wound is clean and dry

and the edges are approximated.

 Secondary Intension Healing- the wound or defect

is larger and gaping and has necrotic or dead
material.

Nursing Management (STRESS)

 • Promoting a Healthy Lifestyle

• Enhancing Coping Strategies

• Teaching Relaxation Techniques

• Progressive Muscle Relaxation

• Benson’s Relaxation Response

• Relaxation with Guided Imagery

Pain

• Pain- is whatever patient says it is and whenever the patient

says it does.

o It is an unpleasant sensory and emotional experience

resulting from actual or potential tissue damage.

• Types of Pain

o Acute Pain-usually recent onset and commonly

associated with a specific injury.

 Usually last for seconds to 6 months

o Chronic Pain- is constant or intermittent pain that

persists beyond the expected healing time and that can
seldom be attributed to a specific cause of injury.

 Last for 6 months of longer.

• Cancer-Related Pain- can be acute or chronic.

Pain Assessment and Management

• Characteristics:

 Intensity- Pain scale: Mild 1-2; moderate 3-5;

severe 7-9

 Timing- threshold-amount of force for patient to

feel pain; tolerance- amount of pain the patient
can bear.
  Onset and Duration- e.g. sudden, intermittent,
gradual.

 Quality- e.g. burning, aching, throbbing,

stabbing.

 Location- local, referred, radiating, projecting.

 Personal Meaning

 Aggravating and Alleviating Factors

 Non verbal behavior

• Role of Nurse

 Identify Goals

 Establishing Nurse-patient relationship

 Provide physical care

 Managing anxiety r/t pain

• Pharmacological Management

o Balance Analgesia

 S/E: Respiratory Depression,

Sedation, N/V Constipation,
inadequate pain relief, pruritus,
tolerance, dependence, addiction

 NSAID

 Opiod/Narcotics (Smeltzer, Bare, Hinkle, &

Cheever, 2008)

 Local Anesthetics

 Topical

 EMLA cream

 Lidocaine 5% patch

• S/E: irritation

 Spinal anesthesia

• S/E: Hemorrhage, infection

 o Pro-Re-Nata/PRN Analgesic

o Preventive Approach

o PCA/Patient controlled analgesia

• Non pharmacologic Management

o Massage/ cutaneous stimulation

o Thermal therapies

o Distractions

o Relaxation

o Guided imagery

o Hypnosis

o Music therapy

o Acupuncture

*Intractable pain

*Neurosurgery

Rhozotomy- destruction of sensory nerve roots

Cordoctomy- cutting of spinal pathways in the spinal

cord.
 Pathophysiology

(Stress, Inflammation, Pain, CHF, Angina Pectoris, Myocardial

Infarction)

Stress

• Stress

o Changes in Environment

o Perceive as challenging, threatening, danger

o Any event, any stimulus, circumstances

Autonomic Nervous
System

Sympathetic Nervous
System
Adrenergic-E/N
Fight or Flight- user of
energy
Aggressive or Avoidance
Increased Activity
Parasympathetic Nervous
System
Repose, vegetation
Cholinergic-Ach
Decreased activity-source
of energy

Organs SNS PNS

Blood Vessels Constriction Dilation
Vital Signs Increased Decreased
Pupil Dilate Constrict
Airways Dilate Constrict
 Blood vessels: GI & Constrict Dilate
GU
Salivation Decreased Increased
Sphincters Contract Relax
Blood Glucose increased No effect

Pathophysiology:

STRESS

STIMULATION OF THE ANS

Stimulation of the hypothalamus

SNS PPG
APG

SAMR

Adrenal Medulla release of ADH

Adrenal Cortex

Increased ADH
Glucocorticoid
N/E E Mineralocorticoid

Increased Blood Volume

Release of
Renin Stimulati ACTH aldosterone
on of the
adrenergIncreased BP and Increased P
ic
Release of receptor cortosol
Reabsorption
angiotensinogen in the
of Na+

catabolism
Convert to
Tachycardia Water
angiotensin reabsorption
CHO CHO
I
N

Fats Increased Bld.

Convert to vol
vasoconstriction Bld. Vol.
angiotensin
II Inflammation BP
Glucose

• Inflammation

• Nonspecific defense of the body

• Nonspecific stimulus of a body that makes

body adaptive

• Neutralizes the effect of the injury

• Prepares body for repair

• Eliminate source of injury

o Selye’s Theory of Adaptation

o GAS

• Neuroedocrine response

• SNS response

• Alarm- increased V/S, decreased resistance

• Resistance- normal V/S, increased

resistance

• Exhaustion-R-est; R-ecover; R-IP.

o LAS

• Nonspecific

• Inflammation

• Pain

Pathophysiology:

Inflammants

(physical, chemical, biological)

 Injury

Vasoconstriction

Release of chemical mediators

(PGE, H, serotonin, bradykinin, leukotrienes)

Vasodilatation

Increased capillary permeability

Fluid/ plasma exudation hyperemia

Swelling (Tumor) Warmness

Redness

(Calor)
(Rubor)

Pain (Dolor)

Loss of Function (function laissa)

Systemic manifestation:

• Fever

• Leukocytosis

• Increased erythrocyte sedimentation

• Headache

• Fatigue

• Malaise
 • Anorexia

Pain

• Pain- is what every person or experiencing person say it

existing whenever the person say it does.

• IASP- Pain is the 5th vital sign

• Set of sensory and emotional response to actual or

potential tissue damage.

Pathophysiology:

Stimulus
-acute
-fast
-
Nociceptors - - - - - - - - - - - - a-delta
Myelinate
d
-chronic
-slow
C-fiber -
unmyelinate
d

Secondary Neuron

Spinal Cord

Afferent neuron

Anterior and lateral spinothalamic tract

Cerebral cortex (fast) Thalamus (slow)

Reticular Formation
 Efferent neuron

Response

CV D/O

• CAD

o CHF

o MI

o Angina Pectoris

• Etiology: Atherosclerosis- hardening and narrowing of

the BV

Risk Factors:

Non-modifiable Modifiable Aggravating

(predisposing (precipitating
factors) factors)
Gender Environment Stress
Age Diet Lifestyle
heredity Condition Obesity

o CHF
o Decreased supply and increased demand of bld.
o Decreased bld. Vol.

o Compensatory mechanism
• Tachycardia
• Ventricular dilatation
• Ventricular hypertrophy
o S/Sx
• DOB
• Rales
• Cough
• Sputum
• Tympanic
Pathophysiology:
Increased residual vol.

CO preload

O2 atrial dilatation

Tissue hypoxia atrial

hypertrophy

Increased atrial
pressure

Backward flow of bld. Towards

lungs

Pulmonary
congestion

Left sided heart

failure

Increased pulmonary
pressure

Backward flow of bld.

Towards right ventricle

Increased pressure
in the right ventricle

Right ventricular hypertrophy

Right ventricular
dilatation

Increased
pressure in the Right atrium

Right atrial dilatation

S/Sx of RCHF Right atrial hypertrophy

Increased CVP
JVD Increased central venous
CNS Depression pressure
Increased ICP
Hepatomegaly Backflow to organs
Slpeenomegaly
Anorexia
N/V right congestive heart failure
Ascites
Portal
hypertension
edema
 Management:

Short acting- nitroglycerine

Long acting- Isosorbide Dinitrate

Nsg. Mngt when giving patches:

Non hairy part

Angina Pectoris

• Pain in the chest wall

• Myocardial ischemia- due to decreased o2

Pathophysiology:
Atheroma

Platelet aggregation narrowing

PGE O2 hypoxemia

Vasospasm cardiac hypoxia

Pain platelet aggregation anaerobic

metabolism

Lactic acid accumulation

Acidosis
MI

• Sudden occultation/obstruction of coronary artery leading to

necrosis

Pathophysiology:

Atheroma

Blockage/ obstruction

No O2 supply

Necrosis

Intense pain increased isoenzymes

Lactic
Increased:
Myoglobin
Dehydroge
nase
Troponin
CPK-MB
S/Sx: (creatine
phospokinase
1. Intense pain

2. Hypotension

3. Tachycardia

4. Tachypnea

5. Fever

6. Indigestion

7. Increased ESR

8. Anxiety

Management:

Morphine SO4 for pain