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 Evento 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 Evento 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 rate and blood pressure

Better perfusion of vital organs

Increased cardiac output due to increased myocardial contractility and heart rate; increased venous return.

Increased blood glucose level

Increased available energy

Increased liver and 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 of skeletal muscles

Preparedness for activity, decreased fatigue

Excitation of muscle; increase in amount of blood shunted to the muscle from the abdominal viscera and skin.

Increased ventilation Provision of oxygen for energy

Stimulation of respiratory center in the medulla; bronchodilation.

Increased coagulability of blood

Prevention of hemorrhage in event of trauma

Vasoconstriction of surface vessels

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 functiono Can adapt to environmental stress through structural and functional

changeso Examples of adaptation

Hypertrophy, atrophy, hyperplasia, dysplasia, metaplasia Reflect changes in the normal cells in response to stress

Maintenance functiono Activities that the cell must perform with respect to itself

Specialized functiono The cell performs in relation to the tissues and organs of which it is a

part

Hypertrophy and atrophyo Lead to the changes in the size of cells

Compensatory hypertrophyo Result of an enlarged muscle mass o Commonly occurs in skeletal and cardiac muscle that experiences a

prolonged, increased workload

Hypertrophyo Increase in the size leading to the increase in organ sizeo Stimulus: increase workloado Example

Leg muscles of runner Arm muscles in tennis player Cardiac muscle in person with hypertension

Atrophyo Can be the consequence of:

a. Diseaseb. Decreased usec. Decreased blood supplyd. Loss of nerve supplye. Inadequate nutrition

o Cell size and organ size decreased

o Structure principally affected:a. Skeletal muscleb. Secondary sex organsc. Heartd. Brain

o Shrinkage in size of cells leading to decrease in organ size

o Stimulus: decrease ina. Useb. Blood supply c. Nutrition

d. Hormonal stimulatione. Innervation

o Example Secondary sex organs in aging person Extremity immobilized in cast

Disuse of a body partso Often associated with the aging process and immobilization

Hyperplasiao 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

Neoplasiao Malignant growtho 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

Metaplasiao 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

Injuryo Disorder in steady state regulationo 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 losto Changes in function ensure

Cause of disorder and injury in the system

o May arise from the internal and external environmento Hypoxia, nutritional imbalance, physical, chemical and infectious

agents, immune mechanisms, genetic defects, psychogenic factor

Most common causea. Hypoxia b. Chemical injuryc. 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 energyc. The ability of the cell to synthesize enzymes and other necessary

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

Homeostatic adjustmentso Concerned with the small changes within the body’s systems

Adaptive changes o Compensation occurso Steady state is achieved (may be a new level)

Hypoxiao Inadequate cellular oxygenationo 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 Imbalanceo It refers to a relative or absolute deficiency or excess of one or more

essential nutrients.

Physical Agentso Temperatureo Radiation and electrical shocko Mechanical trauma

Chemical Agents

o Poison, drugs, alcohol.

Infectious Agentso 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 Inflammationo 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 Regenerationo 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 Paino 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 Managemento 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 Analgesico Preventive Approacho PCA/Patient controlled analgesia

Non pharmacologic Managemento Massage/ cutaneous stimulationo Thermal therapieso Distractions o Relaxationo Guided imageryo Hypnosiso Music therapyo Acupuncture

*Intractable pain*Neurosurgery

Rhozotomy- destruction of sensory nerve rootsCordoctomy- cutting of spinal pathways in the spinal cord.

Pathophysiology

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

Stress

Stresso Changes in Environmento Perceive as challenging, threatening, dangero Any event, any stimulus, circumstances

Organs SNS PNS

Blood Vessels Constriction Dilation

Vital Signs Increased Decreased

Pupil Dilate Constrict

Airways Dilate Constrict

Blood vessels: GI & GU Constrict Dilate

Salivation Decreased Increased

Sphincters Contract Relax

Blood Glucose increased No effect

Autonomic Nervous System

Sympathetic Nervous System

Adrenergic-E/NFight or Flight- user of energyAggressive or AvoidanceIncreased Activity

Parasympathetic Nervous System

Repose, vegetationCholinergic-AchDecreased activity-source of energy

Pathophysiology:STRESS

STIMULATION OF THE ANS

Stimulation of the hypothalamus

SNS PPG APG SAMRAdrenal Medulla release of ADH Adrenal Cortex

Increased ADHN/E E

Increased Blood VolumeRenin ACTH

Increased BP and Increased P cortosol

catabolismTachycardia

Inflammation

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 Adaptationo 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

Stimulation of the adrenergic receptor in the heart

Release of angiotensinogen

Convert to angiotensin I

Glucocorticoid Mineralocorticoid

Release of aldosterone

Reabsorption of Na+

Water reabsorptionCHON CHO

Fats Increased Bld. vol

BP

Glucose

Convert to angiotensin II vasoconstriction Bld. Vol.

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

Nociceptors - - - - - - - - - - - - a-delta

C-fiber

Secondary Neuron

Spinal Cord

Afferent neuron

Anterior and lateral spinothalamic tract

Cerebral cortex (fast) Thalamus (slow)

Reticular Formation

Efferent neuron

Response

CV D/O

CADo CHFo MIo Angina Pectoris

Etiology: Atherosclerosis- hardening and narrowing of the BV

Risk Factors:

Non-modifiable(predisposing factors)

Modifiable(precipitating factors)

Aggravating

GenderAgeheredity

EnvironmentDietCondition

StressLifestyleObesity

o CHFo Decreased supply and increased demand of bld.

-acute-fast-Myelinated-sharp-chronic

-slow-unmyelinated-dull

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

Right atrial hypertrophy

S/Sx of RCHF

Increased CVPJVDCNS DepressionIncreased ICPHepatomegalySlpeenomegalyAnorexiaN/VAscitesPortal hypertensionedema

Increased central venous pressure

Backflow to organs

right congestive heart failure

Management:

Short acting- nitroglycerineLong 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

S/Sx:1. Intense pain2. Hypotension3. Tachycardia4. Tachypnea5. Fever6. Indigestion7. Increased ESR8. Anxiety

Management:Morphine SO4 for pain

LacticIncreased: Myoglobin Dehydrogenase Troponin CPK-MB(creatine phospokinase MB)