6.2. Exam I- Intro, Lymphatic, Immune, Inflam, Cardio, Pulm COMBINED
Introduction to Pathology
Objectives
Define key terms related to pathology.
Analyze the models of health and illness.
Determine the 4 aspects of the biopsychosocial model of pain.
Clarify the genetic aspects of health and illness.
Explain the lifestyle factors that affect health.
Describe health promotion and disease prevention and physical therapy practice implications.
Assess epigenetics and implications for PT practice.
Compare and contrast the increased health risks with obesity and physical therapist practice implications.
Define stress and describe the impact of stress on the organism.
Define and describe various psychiatric disorders.
Discuss the impact of these disorders on the provision of healthcare services to the patient/client.
Describe the role of the physical therapist in addressing the needs of the patient/client with these disorders.
Terms and Definitions: Disease vs. Illness
Disease:
Biologic/Psychologic changes leading to organ or system malfunction.
Biomedical condition(s) indicating disturbances in normal health.
Objective changes.
Can occur without a person being aware of the illness.
Illness:
Perception/response of a person to not being well.
Biologic, personal, interpersonal, & cultural reactions to disease.
A person can feel ill without an obvious pathologic process identified.
Illness: Acute, Subacute, and Chronic
Acute:
Rapid onset & short duration.
Usually self-limiting.
Responds to specific treatment.
Subacute:
Time course between acute & chronic.
Present for > few days, but < several months.
Chronic:
Permanent impairment or disability.
Residual physical or cognitive disability.
Need for rehabilitation and/or long-term medical management. Characterized by several of the above features.
Terms and Definitions: Incidence vs. Prevalence
Incidence:
Measurement of the # of new cases of a disease during a particular period of time.
Measures rate of occurrence of disease.
Leads to probability (risk) of being diagnosed with a disease during a given period of time.
Prevalence:
Refers to the total # of cases of a disease in a population during a specific time period.
References how widespread a disease has become.
Indicates impact of disease on population.
Includes length of time disease has been encountered & includes old/new cases.
Etiology and Clinical Manifestations
Etiology: Cause(s) of a disease or condition.
Clinical Manifestations:
Symptoms (subjective).
Signs (objective).
Morbidity, Premorbidity, and Comorbidity
Morbidity: Diseased state or symptom.
Premorbidity: State of function prior to disease.
Comorbidity: > 1 disease at the same time.
Mortality and Mortality Rate
Mortality: Death.
Mortality rate: # of deaths due to disease/total population.
Taken according to age, sex, area, type of disease.
Several types: infant, perinatal, child, maternal, crude, standardized, & age-specific.
Disability (WHO Definition)
Physical and/or cognitive condition that limits a person’s movements, senses, or activities.
World Health Organization (WHO) Definition Covers:
Impairments: problems in body function/structure.
Activity limitations: Difficulty in executing a task/action.
Participation restrictions: Difficulty with involvement in life situations.
Health Promotion
Built on the principles of self-responsibility, nutritional awareness, stress reduction and management, and physical fitness.
Disease Prevention
More cost-effective than treating disease.
3 branches of preventive medicine:
Primary – Remove or ↓ disease risk factors.
Secondary – Promote early detection, initiate preventive measures for complications.
Tertiary – Limit impact of established disease.
Primary, Secondary, and Tertiary Prevention Examples
Primary:
Good nutrition, calcium & D3 intake, regular weight-bearing exercises, not smoking to prevent osteoporosis.
Secondary:
Skin tests for TB, mammography, colonoscopy, routine cervical Pap smear.
Tertiary:
Rehabilitation to return to the highest level of function.
Disease Prevention & Physical Therapy
Earlier PT intervention → decreased acute care length.
Major roles in secondary & tertiary care.
Secondary: Wide range of settings from hospitals to preschools.
Tertiary: highly specialized, complex, & technologically based settings.
Prevention/Wellness Role:
Prevention/wellness activities.
Screening programs.
Promotion of positive health behaviors.
Impact of Physical Therapy
Clinical Models of Health
Biomedical Model
Model for centuries.
All illness due to disease and physiologic processes.
Psychologic, social and spiritual influences independence of disease.
Focuses on internal factors only.
Illness is a deviation of the healthy state.
Biopsychosocial Model
Biologic, psychologic, and social variables are key factors in health and illness.
Mind and body cannot be separated.
Psychologic factors include cognition, emotion, motivation, along with biologic/environmental factors = various health states.
Family, community, and society interactions influence health outcomes.
Biopsychosocial-Spiritual Model
Developed with the advent of holistic health.
Recognizes the healing potential of faith, spirituality, and religious beliefs.
Social and spiritual support are important for the promotion of health, decreasing susceptibility to disease, and facilitating recovery.
Social-Ecologic Model
Theoretical principles for understanding interrelations among diverse personal and environmental factors in health and illness.
Health is affected by the interaction between the individual, group/community, and physical, social, political environments.
Epigenetics: Behavioral, Social, Environmental Factors and Health Implications
Epigenetics: Study of how behaviors and environment can cause changes that affect the way genes function.
Based on the Social-Ecological Model of Health.
Describes heritable mechanisms that are reversible.
Occurs without alteration of underlying DNA sequence.
The expression of DNA and subsequent reading of the gene can be altered or manipulated.
The mind is considered the "master controller" of gene expression.
Change occurs by becoming aware of individual perceptions, beliefs, and attitudes, behaviors, and lifestyle choices.
Goodman and Fuller Chapter 2.
Epigenetics and Role of Physical Therapist
Epigenetics: Lifestyle Factors Influencing Health
Cultural influences
Socioeconomic status
Generational Differences
Adverse childhood experiences
Physical activity
Nutrition
Obesity
Smoking/tobacco use
Alcohol/drugs
Domestic abuse
Epigenetic Factors Influencing Health
Individual
Family
Community
Society
Physical Therapist Practice Implications
Co-morbidity with referral to PT.
Understanding & sensitivity of symptoms.
Understanding and removal of biases.
Plan of care and goals.
Include patient in goal setting.
Repetition of intervention implications.
Recognize for referral when not diagnosed.
Lymphatic System
Overview
The lymphatic system plays a key role in:
The immune system.
Fluid balance.
Absorption of fats and fat-soluble nutrients.
It moves fluid from the periphery to central circulation, maintaining fluid balance between blood and tissues (fluid homeostasis).
It is part of the body’s immune system and:
Fights infection.
Assists in the removal of cellular debris and waste products.
It absorbs fats/fat-soluble nutrients from the digestive system and transports these fats to blood circulation.
Function
90% of extracellular fluid re-enters circulation via the venous capillary system.
Approximately 2 liters of fluid leak from the cardiovascular system into body tissues daily.
The remaining 10% returns to the heart via the lymphatic system.
This includes fluid and larger protein molecules too large for the venous system (lymph).
It operates as a pressure-driven system based on osmotic diuresis.
Fluid is drained progressively towards larger vessels to lymphatic ducts.
Disruptions to the normal lymphatic transport mechanism lead to accumulations of water/protein in tissue space.
Lymph Nodes
All lymph passes through lymph nodes.
Lymph nodes act as filters to cleanse the lymph of waste products and cellular debris.
Nodes produce lymphocytes and macrophages critical for immune function; they destroy foreign bacteria, viruses, and cancer cells and filter waste products.
Vessels distal to nodes are called afferent lymph vessels, while vessels leaving lymph nodes are called efferent lymph vessels.
Lymphatic Ducts
Lymph empties into the Right Lymphatic Duct and Thoracic Duct.
Lymph returns to the bloodstream via the Left and Right Subclavian Veins.
Cervical Lymph Nodes
Located throughout the head and neck.
Drains fluid from the head and neck.
There are approximately 300 cervical lymph nodes.
Axillary Lymph Nodes
Located around the axillary region.
Drains from upper extremities (UEs) and the upper quadrant.
There are approximately 30 axillary lymph nodes.
Inguinal Lymph Nodes
Located in the upper inner thigh.
Drains fluid from lower extremities (LEs), external genitalia, and the lower quadrant.
There are approximately 12 inguinal lymph nodes.
Lymphatic Organs
Thymus:
Produces mature T-lymphocytes important for adaptive immunity response.
Spleen:
Processes damaged blood cells and microorganisms.
Supports immunity.
Tonsils & Adenoids:
Trap pathogens that enter the mouth/nose.
Produce leukocytes.
Peyer’s Patches:
Small masses of lymphatic tissue that monitor intestinal bacteria.
Carries leukocytes and may store beneficial gut bacteria.
Disorders of the Lymphatic System
Lymphangitis: Inflammation of a lymphatic vessel.
Lymphadenitis: Inflammation of one or more lymph nodes.
Lymphadenopathy: Enlargement of lymph nodes.
Lymphedema: Increased amount of lymph fluid in the soft tissues.
Lipedema: Deposition and hypertrophy of subcutaneous fat.
Lymphangitis vs. Lymphadenitis
Lymphadenitis
Acute or chronic inflammation of one or more lymph nodes.
Often painful.
Acute:
Nodes asymmetrically enlarged, tender, warm, reddened.
Chronic:
Nodes are firm, scarred with fibrous connective tissue, without tenderness or pain.
Lymphangitis
Acute inflammation of subcutaneous lymphatic channels that causes pain and streaks.
Spreads away from the original infection site toward the lymph node.
Mandibular, cervical, inguinal, and axillary regions are most often involved (in order).
Nodes are generally tender to palpation and enlarged.
Systemic manifestations include fever, chills, malaise, and anorexia.
Lymphadenopathy
Swelling/enlargement of lymph nodes.
Secondary to a wide range of bacterial, viral, or fungal infections, autoimmune disease, and malignancy.
Not always inflamed or painful.
Can be localized or regional (enlargement in a particular body area) or generalized (enlargement of 2 or 3 noncontiguous lymph node groups).
Dermatopathic: associated with skin disease.
Treatment depends on the underlying cause (infections, lymphomas, leukemia).
Lymphedema
Swelling of soft tissues from the accumulation of protein-rich fluid in extracellular spaces.
Caused by decreased lymphatic transport capacity and/or increased lymphatic load.
Most common in extremities.
Two broad categories:
Primary (idiopathic).
Secondary (acquired).
Severity graded using a scale from the International Society of Lymphology.
Stages of Lymphedema
Stage 0 (Latent Lymphedema):
Lymph transport capacity reduced.
No clinical edema is present.
Stage I:
Accumulation of protein-rich, pitting edema.
Reversible with elevation: the area affected may be a normal size upon waking in the morning.
Increases with activity, heat, and humidity.
Stage II:
Accumulation of protein-rich, nonpitting edema with connective scar tissue.
Irreversible; does not resolve overnight; increasingly more difficult to pit.
Clinical fibrosis is present.
Skin changes present in severe Stage II.
Stage III (Lymphostatic Elephantiasis):
Accumulation of protein-rich edema with a significant increase in connective and scar tissue.
Severe nonpitting fibrotic edema.
Atrophic changes (hardening of dermal tissue, skin folds, skin papillomas, hyperkeratosis).
Primary vs. Secondary Lymphedema
Primary:
Approximately 15% present at birth.
Most common form occurs from adolescence to midlife.
The exact cause is unknown and NOT linked to any significant traumatic event.
Most likely the result of malformation of lymphatic vessels is present at birth, with 3 types of malformation:
Aplasia: lymphatic collectors are so few and considered absent.
Hypoplasia: < normal expected # in the affected region, or collectors are present but not functional (most common).
Hyperplasia: grossly dilated & enlarged lymphatics.
Secondary:
Results from damage to lymphatic vessels or nodes from a known entity.
The most common cause worldwide is filariasis (a parasitic infection carried by mosquitoes in Africa, South America, India, and Malaysia).
The most common cause where the filaria parasite does not exist is invasive procedures used in the diagnosis & treatment of cancer, regional lymph node dissection, or local radiation treatment.
Other causes: bacterial/viral infections, multiple abdominal surgeries, trauma or surgery that impairs lymphatics, repeated pregnancies.
Crush injuries, compound fractures, severe lacerations, degloving injuries.
Clinical Manifestation of Lymphedema
Swelling of part or all of the affected part.
A feeling of heaviness or skin tightness.
Restricted range of motion: decreased flexibility.
Aching, discomfort, burning, and pain.
Recurring infections.
Hardening and thickening of the skin (fibrosis).
Increased circumferential limb girth.
Postural changes.
Neuromuscular deficits.
May lead to functional changes.
Complications of Lymphedema
Progression of lymphedema leads to thickening of the dermal skin layer, which causes the skin to dry and crack, often leading to ulcerations.
Decreased oxygen delivered to body parts.
Decreased ability to heal.
Skin folds and tissue flaps can develop, leading to the development of fungal and bacterial infections, further skin damage, and a new portal of entry for bacteria.
Increased girth and weight lead to changes in gait pattern with increased fatigue and inactivity, leading to decreased functional ROM and strength.
Physical Therapy Examination and Evaluation
Past Medical History VERY important.
Description of skin integrity (more to be learned from Dr. Gibbs’ integumentary lecture); presence of edema or fibrosis; location & condition of scars, fibrotic areas, open wounds; evidence of healed ulcerations.
Signs/symptoms of cording.
Photographs help detail changes.
Evaluation of function, strength, ROM, balance, and gait.
Circumferential measurements.
Volume measurements.
Bioimpedance spectroscopy.
Physical Therapy Interventions
Manual Lymph Drainage (MLD).
Compression Bandaging (More detail from Dr. Gibbs on bandaging and garments).
Compression garments.
Exercise.
Intermittent Pneumatic Compression Pumps.
Patient Education (basic anatomy, skin/nail care, self-MLD, self-bandaging, garment care, infection management).
Home Program.
Guidelines for Job & Lifestyle Modifications.
Psychologic & emotional support.
Immune System
Learning Objectives
Identify terms/definitions associated with the immune system.
Discuss types of immunity and related functions.
Explain immune system responses.
Recognize organs of the immune system and their functions.
Compare and contrast different classifications of immune disorders and their signs/symptoms, including clinical applications.
Terms & Definitions
Immunology: Study of physiologic mechanisms allowing the body to recognize and neutralize/eliminate pathogens & other foreign components.
Immune System: Network of specialized organs peripherally and centrally providing immediate warning & action against pathogens and foreign substances.
Purpose:
Control or eradicate pathogens/foreign substances.
Protect from disease.
Immunity: Protection against infectious disease (innate & adaptive).
Pathogen: Foreign organism capable of producing disease (bacteria, viruses, fungi).
Phagocytes: Leukocytes that protect the body by ingesting (phagocytosing) harmful foreign particles, bacteria, and dead or dying cells.
Phagocytosis: Process used by cells to engulf and ingest particles of nutrients or bacteria.
Antigen: Molecule attached to a pathogen, located in the pathogen cell wall, stimulating the production of an antibody.
Antibody: "Immunoglobulins" produced by B-lymphocytes (plasma cells). Antigen-specific, binding to and destroying specific antigens (lock & key method).
Innate Immunity
Present prior to exposure; encoded in genome.
Mediates the first line of immunological defense against pathogens (quick response).
Provides a broad range of protection and recognizes any invading pathogen.
Non-specific interaction with different antigens.
Receptors recognize general patterns of common pathogens.
Lacks immunologic memory.
External & Internal Innate Immunity response
Exterior Defenses:
Skin, mucosa, secretions, nasal hair, ear wax.
Internal Defenses:
Soluble Factors:
Complement system, immune mediators.
Cellular components: phagocytes (leukocytes: white blood cells)
Produced in bone marrow.
Neutrophils, macrophages/Monocytes, basophils, mast cells.
Natural Killer Cells.
Soluble Factors
Complement System (complement cascade):
small proteins synthesized by the liver.
Mark pathogens, attracting WBCs and other immune cells from the blood = “complements" their ability to destroy pathogens.
Dissolve cell walls of bacteria → cell death.
Destroy virus envelopes.
Destroy cells infected by viruses.
Enhance strength/activity of innate & adaptive responses.
Functions:
Enhances the ability of antibodies/phagocytic cells to clear microbes.
Promotes inflammation.
Attacks pathogen’s cell membrane → cell lysis.
Final outcomes:
Final smaller proteins of cascade attach to the surface of the pathogen → increased inflammatory response.
Opsonization: Tag pathogen → more susceptibility to phagocytosis.
Forms membrane attach complex → attaches to pathogen membrane → causes pathogen lysis.
Enhances removal of immune complexes formed by antibody/antigen binding.
Soluble Factors: Immune mediators
Restrict proliferation of pathogens.
Cytokines: Cell signaling soluble proteins → signal the immune system to activate.
Stimulate movement of cells towards sites of inflammation, infection, trauma.
Chemokines: Small cytokines → migration of leukocytes & enhance inflammation.
Actions of cytokines/chemokines: ↑ vascular permeability, ↑ vascular epithelial tissue activation, change blood flow & leukocyte migration, chemotactic properties.
Type I interferons:
Cytokines produced by infected cells.
Limit spread of infection → Protect uninfected cells.
Major Cellular Components of Innate System
Neutrophil
Basophil
Mast Cells
Monocyte
Natural Killer Cell
Macrophage
Cellular Components of Innate System
Neutrophils:
First responder against pathogens.
Increased with infection & inflammation → indicates acute infection.
Monocytes:
Largest of WBCs.
Respond to infections/inflammation → mature into macrophages.
Neutrophils kill pathogens → macrophages “filter” the debris (phagocytosis), kill any large bacteria.
(Neutrophils and Monocytes) Classified as leukocytes (principal families of professional phagocytes)
Eosinophils:
Activated with antigens too large for neutrophils (↑ allergies & parasitic infections).
Basophils:
Granulocytes releasing histamine (vasodilator).
Major role in certain allergic responses.
Mast cells:
Release histamine.
Major role in allergy & anaphylaxis.
Active in wound healing.
Dendrites (Antigen-presenting cell (APC)):
Located in tissue in contact with the external environment.
Skin, nose, lungs, stomach, intestines.
Messengers between innate & adaptive systems.
Processes antigen material → attract adaptive system components.
Natural Killer Cells:
Large cytotoxic granular lymphocyte.
Attacks viral and tumor cells.
Membrane to membrane contact.
Releases enzymes & bores pores in the cell membrane.
Proteins enter → cell death.
Adaptive Immunity
Activated if innate immune response fails to control and eliminate pathogen.
The threat continues at a certain level for a certain amount of time: activation threshold.
Antigen-Specific & has memory.
Goal: recognize threat, promote immune response, destroy invader, establish long-term memory → continually develops throughout lifetime.
Result of active or passive immunity.
Active: Introduction of antigen into the body (naturally and artificially (vaccination)).
Passive: Immune products from immune person transferred to nonimmune person.
Transplacental transfer.
Breast milk.
Immune System Response: 3 Lines Of Defense
First line of defense (innate).
Mechanical & Chemical Barriers.
Inhibits invasion of pathogens.
Second line of defense (innate).
Inflammatory response & phagocytosis.
Third line of defense (adaptive).
Specific immune responses (T & B Lymphocytes).
Adaptive Immunity
Composed of T-lymphocyte & B- Lymphocyte cells.
Two categories:
Humoral Immunity (B-cell immunity).
Antibody-mediated.
Cell-mediated immunity (T-cell immunity).
Humoral Immunity
Protects extracellular spaces.
Mediated by antibodies produced by B lymphocytes.
B cells develop in bone marrow, migrate to blood, spleen & lymph nodes.
Each B-cell is specific for a particular antigen outside the cell → destruction of pathogen.
Rely on Helper T-cells for optimal function.
Help activate B-Cells to secrete antibodies.
B-Cell Immune Response
B-Cells: lymphocytes.
B-Cell function: recognize antigens.
Mature into antibody-producing plasma B-cells or into memory B- cells.
Antibodies: Y-shaped proteins that bind to antigen.
B-Cell breaks down antigen.
Antigen-specific antibodies → neutralize or destroy antigens.
Activate complement system → lysis of pathogen.
Neutralize viruses/toxins released by bacteria.
Stimulates phagocytoses of antigen.
Memory cells enable faster production of antibodies to specific antigens in the future.
Cell-Mediated Immunity (T-Cells)
T-cells: produced in bone marrow and then released to mature in thymus.
Mature T-cells recirculate through the bloodstream & peripheral lymphoid organs constantly.
T-Cells encounter antigen → attach and divide into 4 different variations.
T-cells bind with antigens rather than release antibodies as B-cells do.
Protects against infection by intracellular pathogens (rather than in blood).
Each T-cell makes only 1 kind of T-cell antigen receptor.
Cellular Immune Response
Helper T-cell binds to antigens on cell surface → chemical messengers are released that acitvate:
Activates cytotoxic T-cells, B-cells, macrophages.
Required for most adaptive immune responses.
Cytotoxic T-cells (Killer T-Cells) are activated & bind with antigen → release potent chemical, perforin, that perforates cell membrane.
Cell death by lysis results.
Infection brought under control → regulatory or suppressor T-Cells deactivate Killer T-Cells.
Memory T-cells produced for quick response in the future.
Humoral/Cell Mediated Immunity Differences
Humoral | Cell-Mediated |
|---|---|
B-cells | T-cells |
Antibodies secreted | Antibodies not secreted |
Cells, themselves, bind to antigens | |
Destroys extracellular microorganisms | Destroys intracellular organisms |
Antibodies used for defense | Receptors used for defense |
Immunodeficiencies
Immune response is absent or depressed.
Categories:
Primary Immunodeficiency Diseases.
Secondary Immunodeficiency Disorders.
Iatrogenic Immunodeficiency.
Human immunodeficiency virus (HIV).
Chronic Fatigue syndrome.
Immunodeficiencies types
Primary Immunodeficiency:
Group of over rare, chronic disorders.
Congenital defect involving T cells, B cells, or lymphoid tissues, NK cells, phagocytic cells, and complement proteins.
Failure of organ development necessary for lymphocyte maturation or born without certain antibody types.
Indications: Infection that is severe, persistent, unusual, recurrent, or runs in the family.
Secondary Immunodeficiency:
Also referred to as Acquired Deficiencies.
More frequent than Primary Immunodeficiencies.
Results from underlying disease or factor that depresses/blocks immune response: not genetic.
Can occur in malnutrition, stress, CA treatment, leukemia, chronic diseases such as DM & renal failure, undergoing chemotherapy, later stages HIV.
Iatrogenic Immunodeficiency:
Induced by immunosuppressive drugs, radiation therapy, or splenectomy.
Human Immunodeficiency Virus (HIV)
Infection or gradual weakening of the immune system.
Occurs with the exchange of body fluids.
Progressive destruction of T4 (Helper T-cells) lymphocytes (CD4 cells): major regulators of immune response.
HIV unique: some virus escapes despite immune responses.
Slow growth of the virus between acute infection & onset of symptoms.
Untreated → profound immunosuppression results → susceptibility of opportunistic infections (ex. Unusual cancers, tuberculosis, etc.).
Advanced or late-stage HIV disease → formally known as acquired immune deficiency syndrome (AIDS).
Immunodeficiency → infections & unusual malignancies.
Pain Syndromes, musculoskeletal & Neuromuscular/neurologic, cardiopulmonary, integumentary diseases.
No cure but considered the manageable chronic condition (with RX) with medications.
HIV & Rehabilitation
May not be diagnosed: Importance of examination/evaluation.
Standard precautions.
Plan of Care based on HIV disease status & impairments.
Focus on the management of specific impairments & functional limitations.
Pain management.
Balance & Gait training.
Posture, body mechanics.
Stretching & strengthening → do not over fatigue.
Exercise à Improve function.
Chronic Fatigue Syndrome
prevalences among adults in the US.
Fatigue may worsen with physical/mental activity, does not improve with rest.
Cause: unknown → difficult to diagnose.
Theories: triggered by a combination of factors -- hormonal imbalances (thyroid, cortisol), viral infections (Epstein Barr), weakened immune system, psychological stress.
Treatment focuses on symptom relief.
Medical tests are needed to rule out other health problems.
CFS Diagnosis Criteria
Severe chronic fatigue for > consecutive months not due to ongoing exertion or other medical conditions associated with fatigue (These other conditions must be ruled out after diagnostic testing).
Fatigue significantly interferes with daily activities/work.
Individual concurrently has or more of symptoms. These symptoms must have been persistent or recurred during > months of illness and did not predate fatigue.
8 Symptoms that must be concurrent with the first 3 criteria:
Post-exertion malaise lasting > hours.
Nonrestorative sleep.
Significant impairment of short-term memory/concentration.
Muscle pain.
Joint(s) pain without swelling/redness.
Headaches of new type/pattern/severity.
Tender lymph nodes neck/armpit.
Sore throat that is frequent/recurring.
Exercise & Chronic Fatigue Syndrome
Controlled and graded moderate exercise.
Home exercise program: Begin with low-level, intermittent physical activity throughout day = minutes/day.
Assess conditioning, breathing patterns, posture, biomechanics.
Stretching, strengthening, cardiovascular training.
Progress slowly as indicated by tolerance of plan of care.
Monitor vital signs.
Hypersensitivity Disorders
Exaggerated or inappropriate immune response.
Type I – typical allergies → anaphylactic hypersensitivity.
Type II – cytotoxic reaction; rejection of blood transfusions or autoimmune hemolytic anemia.
Type III – immune complex mediated.
Type IV – Delayed hypersensitivity response: contact dermatitis, poison ivy, latex.
Type I Hypersensitivity
Hypersensitivity response produced in response to an allergen.
Allergen: Special class of antigens that cause allergic response.
Examples: hay fever, allergic rhinitis, urticaria (hives), extrinsic asthma, and anaphylactic shock.
Typically genetic predisposition; Reaction occurs within min of exposure. Due to histamine release.
Typical Symptoms: redness, swelling, itching, rhinorrhea.
Most pronounced symptoms present in the upper respiratory tract, GI tract, and dermis.
Anaphylaxis
Widespread release of histamine à systemic response to an allergen that leads to systemic vasodilation, bronchospasm, increased mucus secretion, and edema à anaphylaxis.
LIFE THREATENING!!! Must have injection of epinephrine to restore blood pressure, strengthen heartbeat and restore airway clearance.
The most common trigger of anaphylaxis: bee stings (other triggers = penicillin, foods, animal dander, latex).
Type II Hypersensitivity
2 types: self-recognized as non-self & cross-reaction.
Self-recognized as non-self:
An immune response that is disproportionate or exaggerated relative to the triggering factor.
Excessive & undesirable cytotoxic reactions to self-antigens.
Cellular membrane of normal tissues is disrupted & destroyed.
Usually limited to one type of tissues or organ.
Disorders: blood transfusion reactions, newborn hemolytic disease, some forms of anemia, certain platelet disorders, some types of tissue transplant rejection.
Type II Hypersensitivity: Cross-Reaction:
Cross-reaction between exogenous pathogens & endogenous body tissues.
Examples:
Immune system attacks hemolytic streptococci but also misinterprets mitral valve as foreign streptococci microorganism.
Attack of peripheral nervous system as nonself, as in Guillain-Barre syndrome.
Signs/symptoms:
General: malaise, weakness.
Dermal: hives, erythema.
Respiratory: sneezing, rhinorrhea, dyspnea.
Airway: hoarseness, stridor, tongue and pharyngeal edema, dyspnea, bronchospasm, asthma, chest tightness, wheezing.
Gastrointestinal: increased peristalsis, vomiting, dysphagia, nausea, abdominal cramps, diarrhea.
Cardiovascular: tachycardia, palpitations, hypotension, cardiac arrest.
CNS: anxiety, seizures.
Type III Hypersensitivity
“Immune Complex Disease”: antigen-antibody complexes are deposited in tissues rather than cleared from the body.
Produces inflammatory response and cause local tissue injury.
Common sites of Deposition: skin (urticaria), joints causing synovitis (RA), vasculature (vasculitis), kidneys (nephritis), pleura (pleuritis), and pericardium (pericarditis).
Underlying contributor to systemic lupus erythematous (LUPUS) Inflammatory disorder of connective tissue.
Signs/symptoms:
Headache.
Chest pain.
Back pain.
Tachycardia/hypotension.
Hematuria.
Nausea/vomiting.
Type IV Hypersensitivity
Delayed hypersensitivity response.
Examples: contact dermatitis (cosmetics, detergents, poison ivy, adhesives); transplant rejection.
PT related Possibilities: gels for ultrasound, lotions for soft tissue manipulation, latex gloves.
General signs/symptoms:
Itching, erythema, vesicular lesions on the skin.
Fever.
Arthralgias.
Lymphadenopathy.
Urticaria.
Anemia.
Autoimmune Conditions
Definition: category of conditions with inability of body to distinguish self from non-self, causing the immune response to attack the body’s own tissues – the mistaken reaction of the immune system toward body’s own tissues.
Disruption of immunoregulatory mechanism.
Underlying hypersensitivities may contribute to autoimmune diseases.
Hypersensitivity refers to an immune response that is disproportionate or exaggerated relative to the triggering factor.
Most Common Examples of Autoimmune Diseases
Rheumatoid arthritis
Psoriasis
Systemic lupus erythematosus
Graves’ disease
Inflammatory bowel disease
Hashimoto’s thyroiditis
Multiple sclerosis
Myasthenia gravis
Type I diabetes
Fibromyalgia
Guillain-Barre syndrome
Addison’s disease
Etiology of Autoimmune Diseases
Genetic Predisposition: multiple genes underlie multiple autoimmune diseases
Gender-Specific Hormones Imbalances
Exposure to Certain Viruses: carry structurally similar antigens to self- antigens
Environment: infection, climate, stress, occupation, cigarette smoking
Cross-Reactive Antibodies: antibody for one specific antigen has affinity toward a different one
Silicone Gel Breast Implants
Autoimmune Diseases
Over autoimmune diseases identified.
Spectrum of disorders: single organ involvement (pancreas in type 1 DM) to multi-system involvement (Multiple sclerosis).
Pathogenesis
Disruption of immunoregulatory mechanism → normal cell-mediated & humoral immune responses to turn self-destructive → tissue damage.
Genetic, hormonal, environmental influences.
Clinical Manifestations
Synovitis, pleuritis, myocarditis, endocarditis, pericarditis, vasculitis, myositis, skin rash, alterations of connective tissues, & nephritis.
Fatigue, malaise, myalgias, arthralgias.
Organ Specific Autoimmune Disorders
Addison’s Disease: adrenal cortex insufficiency – too little hormones released widespread metabolic disturbances (hypoglycemia, exhaustion, nausea/vomiting, anorexia, hypotensive).
Graves’ disease:
Hyperthyroid condition.
Autoantibodies stimulate the thyroid → hypermetabolic state.
Symptoms: ↑ sympathetic nervous system, tachycardia, heat intolerance, lipid depletion, ↑ appetite but with weight loss, nutritionally deficient state, and exophthalmos.
Systemic Autoimmune Diseases
Multiple Sclerosis:
Chronic neurodegenerative disorder of the central nervous system (CNS).
Autoimmune cells damage myelin cells → inability to transmit action potentials.
Sclerotic plaques develop throughout CNS.
Myasthenia Gravis:
Fluctuating weakness & fatigability of skeletal muscles.
Receptors at the neuromuscular junction normally receive acetylcholine.
An action potential occurs that leads to muscle contraction.
Antibodies block/destroy acetylcholine receptors at the neuromuscular junction.
Muscle weakness results.
Most common muscles affected: eyes, mouth, throat, face, swallowing.
Systemic Lupus Erythematosus (Lupus):
Definition: Autoimmune, chronic, systemic inflammatory rheumatic connective tissue disease characterized by multiple autoantibodies.
Cause: Exact unknown. Interrelated immunologic, environmental, hormonal, & genetic factors
Clinical Manifestations of Lupus
Musculoskeletal: arthralgias & arthritis.
Cutaneous & membranous lesions:
Skin rash in areas exposed to sunlight (butterfly rash).
Raised, red, scaling plaques.
Vasculitis.
Hair loss (temporary or permanent).
Ulcer in the mouth, vagina, and nasal septum.
Cardiopulmonary: pleuritis, pericarditis, dyspnea, tachycardia, myocarditis, pneumonitis (acute/chronic).
CNS: headache, depression, irritability, emotional instability, psychosis, seizures, CVA, cranial neuropathy, peripheral neuropathy, organic brain syndrome, cognitive dysfunction.
Renal: 50% have renal disease.
Injury, Inflammation, Healing and Repair
Learning Objectives
Describe the mechanisms of cell/tissue injury.
Compare the different means of cellular adaptation.
Explain the cellular responses associated with inflammation.
Describe the process of tissue healing.
Define factors that affect tissue healing.
Compare & contrast the phases of healing.
Cell Injury
Reversible or irreversible.
Factors affecting return to homeostasis:
Mechanism of injury.
Length of time injured without intervention.
Severity of injury.
Mechanism of Cell Injury
Ischemia
Infectious Agents
Immune Reactions (Hypersensitivity, Autoimmune)
Genetic Factors
Nutritional Factors
Physical Factors
Mechanical Factors
Chemical Factors
Mechanisms of Cell Injury - Ischemia
Blood flow below the minimum necessary to maintain cell homeostasis and metabolic function.
blood flow
metabolism
Reduction in oxygen supply (partial: hypoxia, total: anoxia).
nutrients
waste removal
Arterial obstruction and narrowing by atherosclerosis and/or intravascular clot called thrombus.
Mechanisms of Cell Injury - Infectious Agents
Bacteria, viruses, mycoplasma, fungi
Mechanisms of Cell Injury - Immune Reactions
Hypersensitivities
Overactive immune reactions → mild allergy reaction or life-threatening anaphylactic reactions.
Autoimmune
Immune system attacks self.
Mechanisms of Cell Injury - Genetic Factors
Alters the structure or # of chromosomes that leads to multiple abnormalities (Down’s Syndrome/ Trisomy 21).
Single mutations of genes: changes in the amount or functions of proteins (Sickle Cell Disease).
Multiple gene mutations: interact with environmental factors and multifactorial disorders result. (Hypertension, Type II DM).
Mechanisms of Cell Injury - Nutritional Factors
Imbalances in essential nutrients → cell injury or death.
Abnormal levels of vitamins/minerals, protein malnutrition (kwashiorkor), reduced (anemia) or excessive (free radicals) iron.
Mechanisms of Cell Injury - Physical Factors
Trauma: blunt trauma (massive brain contusions, internal organs, blood loss …)
Physical agents: extremes of temperature (burn, frostbite), radiation, electricity
Mechanisms of Cell Injury - Physical Stress
Physical stress exceeds tolerance of the tissue.
Overstretch, compression, friction, anoxia
Mechanisms of Cell Injury - Chemical Injury
Toxic substances lead to chemical injury
Mercury poisoning, agents used in chemotherapy, drug overdose
Types of Cell Injury
Reversible injury: when stress is small and duration is short à cell is able to cover homeostasis after stress removal
Irreversible injury: when stress is of sufficient magnitude or duration à cell is unable to adapt
Adaptation
The ability to alter mechanisms and regain homeostasis in the altered environment by cells or tissues
Alterations with sub-lethal stress over a period of time
Cellular adaptation characteristics:
Change in cell size, #, or function
Increases ability to survive
Cellular Adaptations
Common cellular adaptations
Atrophy: Reduction in cell and organ size due to vascular insufficiency, reduction in hormone levels, malnutrition, immobilization, and pain
Hypertrophy: Increase in size (skeletal muscle, cardiac cell hypertrophy)
Hyperplasia: Increase in # of cells → increased tissue size (uterus during pregnancy, skin callus, prostate enlargement)
Metaplasia: Conversion of an adult cell; change in form or function (smoker respiratory epithelium)
Dysplasia: Pre-neoplastic alteration; ↑ in number with altered cell morphology, and loss of histological organization (chronically injured area)
Inflammation
Normal secondary response to cell injury followed by healing & repair
Viral role in host defense mechanism against pathogens protecting host from infection/injury
Purpose: mobilize & transport the body’s defenses essential for healing to occur
Removal of injurious agent
Removal of cellular debris (dead cells)
Initiation of healing process
Intertwined with process of repair
Stimulates response for healing
Involves complex set of vascular, neurologic, & cellular responses
Acute Versus Chronic Inflammation
Acute Inflammation
Sudden onset with short duration; self limiting
Exudation of fluid and plasma protein (edema), migration of leukocytes (neutrophil)
Clinical manifestations: redness, swelling, increased temperature, pain, decreased function, increased Muscle Tone or Spasm
Chronic Inflammation
Long duration: weeks, months, or years
Causes:
Extensive necrosis
Underlying cause not addressed
Chronic overuse
Repeated trauma
Low-grade, persistent immune reactions
Autoimmune diseases
Hallmark in tissue: accumulation of macrophages, lymphocytes, & plasma cells
Much greater scar formation
Components of Inflammatory Response - Vascular alterations
Vasoconstriction of small arteries supplying injured area
Due to neural reflex
Short duration, ~ 10 minutes
Vasodilation
Long duration
blood flow to injured area (thus blood volume) → hydrostatic pressure
Transudation results: leakage of low-protein fluid from vasculature into the injured tissue (transudate)
Erythema, warmth, and edema
Exudation: extravascular fluid with high-protein
Components of Inflammatory Response - Leukocyte Accumulation
protein & fluid in vasculature (due to transudation) → engorgement of red blood cells in vessels → stasis
Stasis: slowing or cessation of blood flow
During stasis, leukocytes accumulate and adhere to endothelial cells of blood vessel walls at injury site (margination)
Actively pass through the vascular walls, migrating out of vessel into interstitial space without damage to vessel wall (diapedesis or oozing)
Diapedesis due to leukocytes attraction to chemotactic agents in interstitial space at site of injury (chemical stimulus)
Leukocyte locomotion process: chemotaxis
Summary of Inflammatory Response
Tissue Injury → Vaso Constriction → Vasodilation → Transudation → Stasis → Margination → Diapedesis → Chemotaxis → Phagocytosis
Chemical Mediators
Responsible for the vascular & leukocyte responses with acute inflammatory response
Released from inflammatory cells or plasma
Cell-derived – generated from inflammatory cells
Plasma-derived – generated by plasma protease (enzymes that act as catalyst in breakdown of proteins)
Multi-functional effects on blood vessels, inflammatory cells, other body cells
Vasodilation, vasoconstriction, vascular permeability change, activation of inflammatory cells, chemotaxis, cytotoxicity, affect fever & pain
Cell-Derived Mediators
Histamine
Endothelial Contraction - Increased membrane permeability
Vasodilator (Strong)
Potent bronchoconstrictor
Stored in mast cells, basophils, platelets
Serotonin
Vasoconstriction
Effects overridden by histamine
Cytokines
Wide range of inflammatory actions & systemic actions
Moderate activity/function of other cells
Prostaglandins
Lipids made at sites of tissue damage with hormone-like effects
Mediators of fever/pain responses associated with inflammation, constriction or dilation blood vessels
Clot formation
Chemokines
Specific types of cytokines
Chemoattractants for leukocytes, neutrophils, monocytes (direct the leukocytes to the pathogen)
Plasma-Derived Mediators
Blood Coagulation Cascade
Plasma proteins bandage injuries with clots (coagulation)
Disassemble (lyse)
Thrombin → Fibrinogen to fibrin
Fibrinolytic System
Activated by fibrinolysin
Dissolves clots
Bradykinin
Inflammatory Mediator
Peptide that causes vessel dilation and pain
Complement System
Plasma proteins dormant in blood, interstitial fluid, & mucosal surfaces
Activated by foreign protein & antigen-antibody complex
Vasodilation, leukocytes migration, opsonization
Tissue Healing
Begins soon after tissue injury/death
Tissue healing occurs either by regeneration (regrowth of original tissue) or by repair (formation of a connective tissue scar)
Complex and influenced by many components
Components
Fibronectin
Proteoglycans
Elastin
Collagen
Fibronectin
One of the first proteins to provide structural support that stabilizes the healing tissue - most common type of cell in connective tissue
Most important functions:
Formation of scaffold
Provision of tensile strength
“glues” other substances/cells together
Binds to fibrin: protein that makes up blood clots present in injured tissue
Attracts fibroblasts & macrophages by chemotaxis
Stimulated fibroblasts secrete more fibronectin
Binds to proteoglycans and collagens à stabilizes healing tissues
Proteoglycans & Elastin
Proteoglycans
Proteins secreted by fibroblasts early during tissue repair reaction
Bind to fibronectin & collagen: helps stabilize the healing tissue
Aid in hydration of tissue
Collagen
Most important protein to provide structural support and tensile strength most tissues and organs à Give stability to healing tissues
28 different types: each type has special function
Type I: most common form, found in all body tissues, structurally very strong, predominant in tendons/bones & mature scars
Type II: predominant in cartilaginous tissue & bone physis (growth plate)
Type III: provides support for developing capillaries / makes tissues strong but supple, & elastic
Type IV: forms basement membrane to which other cells are anchored
Factors Affecting Tissue Healing
Growth Factors
Proteins that regulate several cellular reactions involved in healing: cell proliferation, differentiation, & migration
Nutrition: vitamin A, vitamin B, vitamin C, zinc, protein, and carbohydrates
Vascular supply
Presence of Infection
Immune reactions
Age
Comorbidities / medications
Smoking
Phases of Healing
Within 24 hours after dead tissue removal:
Hemostasis
Inflammation
Proliferation
Remodeling (maturation)
Hemostasis
Hemostasis is the first step, occurring immediately after acute injury as body tries to stop bleeding
Vessels constrict to restrict the blood flow
Platelets plug formation
Coagulation cascade: formation of blood clot – thrombus
Inflammation
Serves vital role in healing process
Protective and curative features
Begins once blood clot forms
Suffix = “-itis”
Functions
Inactivate injurious agent
Breakdown/remove dead cells
Initiate tissue healing
Proliferation
Reconstruction step with endothelial cell proliferation
Purpose: establish vascular network to transport & nutrients & support metabolism of healing tissue
Characterized by formation of granulation tissue, angiogenesis, wound contraction and process of epithelialization
Occurs 3-5 days following injury
Overlaps with inflammatory phase
Angiogenesis: formation of new blood vessels, involving the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels
Remodeling (Maturation)
OCCURS AFTER 2-3 WEEKS – 2 YEARS
SCAR TISSUE REDUCED & REMODELED: SMOOTHER, STRONGER, LESS DENSE, LESS RED TISSUE
COLLAGEN FIBERS REMODELED: PRODUCED, BROKEN DOWN, REARRANGED – GROWING STRONGER (BUILD TENSILE STRENGTH AND ELASTICITY OF THE SKIN)
3 MAIN REMODELING STEPS: TISSUE CONTRACTION & CONTRACTURE, TISSUE REGENERATION, TISSUE REPAIR
Tissue Contraction & Contracture
Extracellular matrix draws together: healing tissue contracts
Tissue defect size is shrinking
Due to specialized fibroblasts: myofibroblasts that accumulate in wound margins
Tissue contraction approximates the margins of the healing tissue – wound closing
Contracture: excessive shrinkage – can limit mobility
Tissue Regeneration
Regeneration: The process of replacement of dead cells by new cells
Regrowth of original tissue
Restores normal tissue structure and function
Occurs due to healthy cell mitosis (cell division)
Tissue Repair
Most healing involves regeneration & tissue repair
Tissue repair: replacement by connective tissue scar
Dense, irregular laying down of collagen
Occurs with damage beneath epidermis
Scar tissue: 70-80% as strong as original tissue, less vascular
Scar function dependent upon stresses applied during healing
Physical Therapy & Scar Tissue
EXERCISE!
Scar remodeling occurs with stress (stretch/strengthening exercises)
Realignment of collage fibers to become stronger
Pressure
Myofascial release
Deep transverse friction tissue mobilization
Lubrication
Stretching
Kinesiology tape
Therapeutic Pulsed Ultrasound
Cardiac Disease
Learning Objectives
Define normal structure, circulation, and function of the heart.
Recognize signs, symptoms, and risk factors of cardiovascular disease.
Compare and contrast etiology, risk factors, pathogenesis, and clinical manifestations of diseases.
Describe rehabilitation implications for each of the diseases affecting heart muscle.
Discuss differences between sexes in cardiovascular disease.
Conclude when it is appropriate to refer patients with cardiac disease.
Layers of the Heart
Pericardium
Myocardium
Middle muscular layer of the heart.
Primary mover of the heart.
Epicardium
Thin layer of elastic connective tissues and fat.
Contains the coronary arteries.
Endocardium
Most inner layer of the heart.
Lining of the chambers of the heart.
Coronary Arteries
Originate from the aorta and supply blood to the heart.
Left main
Left anterior descending
Circumflex
Right main
Posterior descending
Anatomic Region of Heart & Coronary Artery Association
Inferior: Right coronary artery
Anteroseptal: Left anterior descending
Anteroapical: Left anterior descending (distal)
Anterolateral: Circumflex
Posterior: Right coronary artery
Circulation of Blood through the Heart
Lungs
Pulmonary Veins
Only veins with oxygenated blood
Left Atrium
Bicuspid/Mitral Valve
Left Ventricle
Aortic Semilunar Valve
Aorta
Body Tissues
Vena Cava
Right Atrium
Tricuspid AV Valve
Right Ventricle
Pulmonary Semilunar Valve
Pulmonary Arteries
Valves of the Heart
Atrioventricular
Tricuspid and Bicuspid (Mitral)
Located between the atria and corresponding ventricle.
Bicuspid (Mitral)
Located between the left atrium and ventricle.
Tricuspid
Located between the right atrium and ventricle.
Anterior, Septal, and Posterior cusps
Semilunar
Pulmonary and Aortic
Located between ventricles and corresponding artery.
Pulmonary
Located between the right ventricle and pulmonary trunk.
Left, right, anterior cusps
Aortic
Located between the left ventricle and ascending aorta.
Left, right, posterior cusps
Conduction System
Goal is sequential atrioventricular contraction
SA Node
Internodal Pathways
Atria Contracts
AV node
Ventricles
Bundle of His
Purkinje Fibers
Ventricles contract
Electrocardiogram (ECG)
P wave
Atrial contraction
PR Interval
Seconds from the beginning of the P wave to the QRS segment
PR segment
Conduction through atria and delay of AV node
QRS Complex
Ventricular contraction
T Wave
Ventricular recovery/relax
QT Interval
Time of ventricular contraction and relaxation
Key Terms and Definitions
Blood Pressure
= diameter of vessels and viscosity of blood
Systolic Pressure
Highest arterial pressure of cardiac cycle
Immediately after contraction of left ventricle
Diastolic Pressure
Lowest arterial pressure of cardiac cycle
Occurs between heart contractions
Stroke Volume
Volume ejected after each heart contraction
Influenced by preload, afterload, and contractility (inotropy)
Cardiac Output
Volume of blood ejected each minute
5-6 L/min at rest
Ejection Fraction
Amount of blood left in ventricle per contraction
Normal: 50-70%
Cardiovascular Disease Prevalence
Risk Factors
Hypertension
High serum cholesterol levels
Smoking
Sedentary lifestyle
Poor diet patterns
Overweight/obesity
1 in 4 deaths in the U.S. due to cardiovascular disease
Leading cause of death in the U.S.
Coronary heart disease – most common type of heart disease
~735,000 individuals in the United States have myocardial infarctions each year
Ischemic Heart Disease
Also known as Coronary Artery Disease (CAD) or Coronary Heart Disease (CHD)
Pathology
Narrowed/blocked arteries in the area of heart supplied becomes ischemic/injured
Myocardial infarction may result
Narrowing caused by Arteriosclerosis
Thickening and loss of elasticity of arterial walls
Atherosclerosis
Most common type
Accumulation of fatty deposits in the inner layer of arteries
Coronary Vascular vs. Coronary Artery vs. Cerebrovascular Coronary Artery Disease
Pathogenesis
Arterial wall damage by harmful blood substances and/or hypertension
Injury leads to infiltration of macromolecules such as cholesterol into smooth muscle cells
Platelets attracted
Thrombus formation
Thrombus can rupture, narrow, or block artery
Coronary Artery Disease Risk Factors
Non-Modifiable
Family history
Age (40+)
Sex
Ethnicity
Infection
Chlamydia Pneumonia
Helicobacter pylori
½ US have antibodies for above
Modifiable
Smoking
High Cholesterol
Obesity
Hypertension
Physical Activity
Glucose metabolism
Hormonal status
Psychologic factors
Alcohol Abuse
Coronary Artery Disease Prevention
Atherosclerosis begins in adolescence and young adulthood
Address modifiable risk factors early
Moderate-intensity exercise at least 30 minutes 5-7 days/week
Decreased risk for:
Coronary events
Ischemic stroke
Metabolic syndrome
Insulin resistance
Diabetes
Improves heart rate recovery
Lowers cholesterol levels
Coronary Artery Disease Diagnosis
Cholesterol checks
Begin at 20 and recheck every 5 years
Coronary angiography
X-ray with dye of arteries
Echocardiography
Ultrasound imaging
Stress echocardiography
Exercise treadmill testing
25 – 30 bpm = good, 50-60 bpm = excellent
Abnormal recovery = 4x as more likely to die from CAD
Decline of systolic pressure after graded exercise: correlates with CAD
Coronary Artery Disease Surgical Interventions
Coronary Stents
Drug-coated metal stents with plastic coating
Hold and release drugs that inhibit growth of endothelial cells
Coronary Artery Bypass Graft (CABG)
Portion of vein or artery grafted onto coronary artery
Bypasses blockage
Percutaneous Transluminal Coronary Angioplasty
Opens occluded coronary artery without opening chest
Involves double lumen balloon catheter
Implications for Rehabilitation
Cardiac Rehab Phase 1-3
Inpatient, outpatient, maintenance
Discharge instructions
Sternal Precautions
Indications for Exercise
Sternal Precautions
No pulling up in bed
Must roll side to side
No pushing, pulling, or lifting > 5 to 10 pounds for 6 weeks.
Vacuuming, lifting children bets, moving furniture, opening doors etc.
Move in the tube sternal precautions
No driving
Avoid horizontal abduction and extreme external rotation
Cough with heart pillow for splinting
Avoid using armrests to push up from chair
Angina Clinical Manifestations
Pain or discomfort in chest
Substernal
Occasionally refers to the left scapular area
Patients will report
Squeezing
Burning
Pressing
Heartburn
Indigestion
Choking
Varies in intensity
Can last 1 to 15 minutes
Usually relieved by rest or nitroglycerine
Angina Pathogenesis
Workload exceeds oxygen demand for various reasons
Symptom of ischemia secondary to imbalance between cardiac workload
90% secondary to CAD
Disruption of plaques can lead to occlusive thrombus
Unstable angina or Myocardial Infarction
Types of Angina
Stable or Chronic
Demand ischemia
Involves coronary arteries
Predictable threshold of activity or stress
Hot and cold weather may trigger
5 minutes or less is normal
Use rest or nitroglycerine
Unstable
Unpredictable
Changes in intensity, frequency, or threshold
Lasts longer than 15 minutes
Symptom or worsening cardiac ischemia
Variant (Prinzmetal’s)
Caused by coronary artery spasm
No CAD
Triggers
Stress, extreme weather, vasoconstriction meds, smoking/cocaine
Nitroglycerine and calcium antagonists
Microvascular
Involves coronary microvasculature
Endothelial dysfunction = chest pain
Most often postmenopausal
Most severe and lasts the longest
Often first noticed with ADL’s and emotional stress
Medical Management
Diagnosis
History supported by relief with sublingual nitroglycerin
Long-acting nitrates allow increased exertion
Treatment
Avoid provoking situations
Keep nitroglycerin for acute attacks
Decreases cardiac workload by decreased cardiac oxygen demand
Decreases preload and afterload
Medication to decrease heart rate and force of contraction
Decreased myocardial demand
Anticoagulants for unstable angina
Revascularization procedures
PTCA and CABG
Rehabilitation Implications
Unstable angina requires immediate medical referral
If known, need to have nitroglycerin on hand
Administer and sit down supported or in supine until symptoms resolve
Usually very quick
Watch for orthostatic hypotension
Common side effect of medications
Monitor vitals
Exercise below threshold
May be blunted heart rate responses
Education
Myocardial Infarction
Pathogenesis
Heart attack: development of ischemia with resultant necrosis of myocardial tissue
Heart deprived of oxygen
Leading cause of death among adults in the U.S.
Same etiology and risk factors as CAD
Angina due to CAD is predictive of Myocardial Infarction
80—90% is secondary to coronary thrombus due to the site of preexisting atherosclerotic stenosis
Other causes are cocaine use, vasculitis, aortic stenosis, coronary artery dissection
Vessel becomes partially or completely blocked due to plaque
Clinical Manifestations
Sudden sensation of pressure with crushing chest pain
Often radiates to arm, throat, neck, and back
Pain is constant
30-60 minutes
Up to hours
Pallor, Shortness of breath, diaphoresis
Women
Sudden nocturnal shortness of breath
Chronic, unexplained fatigue
Unexplained anxiety
Indigestion
Silent Myocardial Infarction
Associated with no pain
More common in older adults, all smokers, diabetes mellitus, and women
Vomiting, fever in the first 24 hours and persist for a week
Postinfarction Complications
Arrhythmias
Most common (90%)
Congestive Heart Failure
Pericarditis
Myocardial rupture
Fatal and most often left ventricle
Thromboembolism
Recurrent Infarction
Sudden death
Medical Management
Diagnosis
Clinical history, ECG interpretation, measurement of cardiac enzyme levels
Troponin most common
Treatment
If during treatment – rapid response/code blue or call 911 if outpatient
Chew/swallow aspirin
Nitroglycerin if prescribed
Unlock door
Lied down
Early intervention is optimal
Reestablish blood flow
Acute: thrombolytics
Post-acute: Same as CAD (stints, bypass, angioplasty)
Rehabilitation Implications
Activity recommended with graded progressions
Cardiac rehab can lead to coronary artery collateral growth
Specific dosages of aerobic, resistive, and flexibility exercises
Sexual activity
Follow general recommendations for AHA
Orgasm: Physiologically equivalent to brisk walk/climbing a flight to stairs
5 METS
Early mobilization
Gentle and prevention complications
Usually within 24 hours
Holding breath and Valsalva contraindicated
Monitor vital signs!
Special care
Patients on thrombolytics
Education on precautions/contraindications
Referral for mental health and wellness
Heart Failure
Heart is unable to pump sufficient amount of blood to supply body’s needs
Due to disorders of:
Pericardium
Myocardium
Epicardium
Heart valves
Large coronary vessels
Metabolic abnormalities
May occur on both sides or predominantly one
Usually due to left ventricular dysfunction
Most common reason for hospitalization in ages 65+
Heart Failure Classifications
Left Ventricular Failure
Congestive heart failure
Leads to pulmonary congestion
Acute Right Ventricular Failure
NOT due to other issues
Leads to superior and inferior peripheral system congestion
Cor Pulmonale
Heart disease due to underlying pulmonary condition
Leads to right heart failure
Pathogenesis – Left Heart Failure
First Compensatory Stage
To maintain normal cardiac output – chambers enlarge to hold more blood
Ventricular dilation
Limited dilation before the threshold resulting in decreased contractility
Right ventricle continues as normal
With reduced left ventricular function, a back begins to occur leading to pulmonary congestion/edema
Dyspnea is for all people to some degree.
Second Compensatory Stage
Sympathetic nervous system responds
Stimulation of heart muscle to increase rate
Leads to ventricular hypertrophy
More oxygen is required to maintain increased heart rate
Angina pectoris begins to occur due to ischemia with hypertrophic demands
Third Compensatory Stage
Activation of the renin-angtiotensin- aldosterone system
Kidneys begin to retain water and sodium due to decreased blood
Further tissue edema
Increased load on compromised heart
When this stage finally fails, the patient reaches decompensated heart failure
Right Sided Heart Failure
Often but not always due to left-sided heart failure
Or can be right ventricle weakness and unable to empty
Blood will back up into systemic circulation via superior and inferior vena cava
Peripheral edema in legs, liver, abdominal organs
Ascites
Very high venous pressure causes distention of vessels
Jugular vein distention
Congestive Heart Failure Medical Management
Diagnosis
Clinical diagnosis
Symptom severity
Echocardiogram: primary diagnostic tool.
Treat underlying cause
Diet, exercise, lifestyle
Pharmacologic
Reduce heart workload
Increase cardiac muscle strength and contraction
Diuretics
Surgery
CABG
Cardiac Transplant
Pacemaker
Physical Therapy Implications
Monitor vital signs
Peripheral edema
DO NOT COMPRESS
Assess jugular vein distention
Utilize the Borg Scale
Positioning
Dependent position
Head of bed
Slow progression
Energy Conservation
Patient education
Psychosocial
Heart Valve Diseases
Valve Dysfunctions
Functional
Congenital deformities
Rheumatic fever
Trauma
Ischemia
Prolapse
Enlarged valve leaflets bulge backwards
Mitral or Tricuspid
Anatomic
Insufficiency
Regurgitation when the valve does not close properly
Blood flows back into the chamber
Dilation Occurs
Stenosis
Valve does not open fully
Obstruction leads to chamber hypertrophy
Mitral Valve Stenosis
Mild
Asymptomatic with left atrial pressure and cardiac output remain normal
Moderate
Dyspnea and fatigue appear and left atrial pressure rises
Decreased cardiac output
Severe
High left atrial pressure
Pulmonary congestion at rest
Dyspnea and fatigue, right ventricular failure
Diagnosis
Echocardiogram
Intervention
Pharmacologic: anticoagulants, antiarrhythmic agents
Surgery: valve replacement, balloon valvotomy
Mitral Valve Regurgitation (Insufficiency)
Associated with female, lower BMI, older age
May be asymptomatic until severe left ventricular dysfunction occurs
Exertional dyspnea
Exercise-induced fatigue
Diagnosis
Clinical with auscultation
Echocardiogram
Treatment
Mild – Diuretics, anticoagulants, anti-hypertensives
Moderate-Severe
Valve replacement/repair
Education
Mitral Valve Prolapse
50% are asymptomatic
40% are only mild to moderate symptoms
Fatigue
Palpitation
Dyspnea
Not at greater risk for heart failure
Treatment
Pharmacologic – antiarrhythmics
Exercise
Lifestyle education
Antibiotics before any invasive procedure
Arrhythmias
Ventricular
Fibrillation
Often results in cardiac arrest
Premature
Can be benign but should be documented
Atrial
Fibrillation
Most common and can lead to stroke/failure
Blood clot will originate and travel
Heart Block
Slowing or interruption of impulses from atria to ventricles
Different degrees and types
Treatment
Pharmacology
Many types, will learn more later
Cardioversion
Synchronized electrical shocks
Defibrillation
Ablations
Catheterization threads wire to where arrhythmia originates and the area is destroyed
Pacemaker
Single chamber – right ventricle
Dual chamber – right ventricle and atrium
Biventricular
Resynchronization therapy: used with heart failure
Pulmonary Disease Notes
Impact of Lung Disease
COPD is the 4th leading cause of death in the US.
Over 50% of Americans with lung disease are undiagnosed.
Lung disease directly impacts exercise and ADLs, requiring modifications to physical therapy recommendations.
Smoking statistics:
1960: 55% ♂ / 30% ♀
2008: 22.8% ♂ / 18.5% ♀
2016: 18.6% ♂ / 14.3% ♀
2021: 13% ♂ / 10% ♀
Patients with chronic respiratory disorders are at risk for acute exacerbations, ER visits, hospitalization, and co-morbidities.
Chronic lung disorders result in chronic modification of ADLs and therapeutic interventions.
Leading Causes of Death in US (2021)
1. Heart disease
2. Cancer
3. Medical errors (under-documented)
4. COPD (Chronic lower respiratory disease)
5. Accidents
6. Stroke
7. Alzheimer’s disease
8. Diabetes
9. Influenza & pneumonia
Kidney disease
Pulmonary A&P Review
Upper airways: above larynx (vocal cords); includes nasopharynx, oropharynx, laryngopharynx.
Vocal cords division.
Lower airways: below larynx; includes conducting zone & respiratory zone.
Pulmonary A&P Review (Continued)
Conducting Zone: Trachea -> Bronchi -> Bronchiole -> Terminal Bronchiole (23-24 bifurcations).
Respiratory Zone: Respiratory bronchioles -> Alveolar Duct -> Alveolar Sac -> Alveoli.
Respiratory Zone: Actual interface of alveoli with capillary beds (AC membrane) for exchange of CO2 and O2 with RBCs.
O2/CO2 exchange (respiration).
Gases diffuse from high concentration to low concentration.
orr70 m^2O2/CO2 exchange through A/C membrane in the Respiratory Zone.
Ventilation: mechanical movement of gas in and out of lungs as a function of thorax musculature, lung compliance, and airway resistance.
Control of ventilation: neuro-chemical through carotid bodies and CSF response through BBB.
Hypercapnic drive vs. hypoxic drive.
Ventilatory Muscles
Muscles of resting ventilation:
Inspiration: diaphragm.
Expiration: none (passive recoil of thorax).
Muscles of active ventilation (accessory muscles):
Inspiration: sternocleidomastoid, external intercostals, scalene, trapezius, pectoralis major/minor.
Expiration: internal intercostals, transverse abdominis, external/internal obliques, serratus, latissimus dorsi.
Pulmonary Function Test (PFTs)
Primary method for Dx/stage lung disease.
Total Lung Capacity:
The Volume of Air in the Lungs After a Maximum Inhalation
Tidal Volume:
The Volume of Air Inhaled or Exhaled During Normal Breathing
Vital Capacity:
The Maximum Amount of Air a Person Can Exhale After a Maximum Inhalation
Inspiratory Reserve Volume:
The Maximum Amount of Extra Air That Can Be Inhaled Above Tidal Volume
Expiratory Reserve Volume:
The Maximum Amount of Extra Air That Can Be Exhaled Beyond Tidal Volume
Residual Volume:
The Volume of Air Remaining in the Lungs After a Maximum Exhalation
Pulmonary Signs and Symptoms
Sign (objective finding perceived by examiner) vs Symptom (subjective indicator of disease or change as perceived by the patient).
Cough.
Dyspnea.
Abnormal sputum.
Chest pain/discomfort.
Hemoptysis.
Cyanosis.
Digital clubbing.
Altered breathing patterns.
Digital Clubbing
Fingers & toes.
Altered Breathing Patterns & Sounds
Hyperventilation (hyperpnea vs. tachypnea).
Hypoventilation (hypopnea vs, bradypnea).
Stridor (high-pitched inspiratory sound).
Wheeze (musical expiratory sound).
Crackles (known as rales, crackling inspiratory sound).
Aging and the Respiratory System
Normal physiologic changes.
Senile emphysema (shrinking “tennis court”).
Chest wall compliance decreases (ribs ossification, joints stiffening).
Elastic recoil of lungs decreases (loss of muscle fiber).
Overall decreased ventilatory capacity with reduced VC, increased RV, decreased exercise tolerance (increased DOE and SOB).
Classification of Lung Diseases
Physiology of Restrictive vs. Obstructive Lung Disease.
Both classified/diagnosed through patient Hx, chest assessment, CXR, ABGs, and PFTs.
Restrictive Pulmonary Disease: generally the “inability to take a deep breath
” due to restriction (stiffening) of lung tissue or the thorax or neurological disorder.
Obstructive Pulmonary Disease: generally the “inability to exhale each breath completely
” due to a reduced expiratory airflow from obstruction of the airways.
Obstructive Lung Disease
Acute or Chronic; Reversible or Non-reversible.
Termed COPD in US and COLD in Europe.
Prolonged expiratory time required by patient to empty lungs due to thoracic pressure dynamics.
Following heart disease, 2nd most debilitating disease of adults under 65 and 3rd leading cause of death (Pack-Years > 60).
Environmental irritants cause exacerbations & increase morbidity/mortality rates.
Diagnosis/management of COPD recognized world-wide using Global Initiative for Chronic Obstructive Lung Disease (GOLD) standards through NHLBI and WHO.
Acute Obstructive Lung Diseases
Acute bronchitis: inflammation of trachea and bronchi with a bacterial or viral etiology.
Asthma: potentially reversible obstructive
airways disease caused by increased Raw due to hyperactivity in the presence of personal airway triggers; may potentially return to normal lung function.
Croup and epiglottis: acute obstruction of upper airways.
Chronic Obstructive Lung Diseases
Chronic bronchitis, emphysema, asthma.
Term COPD used when CB and emphysema present concurrently.
Also cystic fibrosis (CF), bronchiectasis, bronchiolitis.
Emphysema
Anatomic Definition: permanent destruction of alveoli, connective tissue, and capillary beds resulting in hyper-inflation (air trapping) with loss of elastic recoil of lung tissue.
Centrilobular: cigarette smoking (60 pack-yrs).
Panlobular: genetic (alpha1-antitrypsin deficiency)
Loss of elasticity and alveoli -> air trapping -> barrel chest (1:1) -> increased WOB/DOE -> weight loss/difficulty eating -> accessory muscle hypertrophy.
Progressive anatomic changes:
Loss of “tennis court” AC interface -> increased pulmonary vascular resistance -> cor pulmonale -> increased pedal edema, palpable liver, JVD’s in neck.
Increased SOB at rest -> increased sedentary lifestyle.
Emphysema PFTs Diagnosis & Staging
Increased lung volumes.
Reduced expiratory flow rates.
Decreased diffusion capacity due to loss of capillary beds.
Limitation of thoracic cage expansion and diaphragmatic excursion.
V/Q ratio near normal due to focused work on breathing. Pursed-lip breathing helps keep alveoli from collapsing. Described as “pink puffer.”
Tx: Disease is progressive with low flow O_2 primary support, possible corticosteroids during exacerbations, inhaled bronchodilators when indicated, when cor pulmonale presents < 6 months survival.
Chronic Bronchitis
Clinical definition: chronic productive
cough for 3 months out of year for 2 consecutive years.
Chronic irritation of airways -> inflammation, edema, excessive mucous production, hyperplastic mucous glands, physical obstruction of large and small airways by mucous, normal mucous clearance impeded due to increased viscosity.
Initially NORMAL alveoli!
Cyanosis “Blue Bloater” characteristics with poor ventilation.
Hypercapnea and hypoxia increase pulmonary vascular pressure resulting in early cor pulmonale.
Polycythemia, digital clubbing, similar PFT changes as seen with emphysema except normal diffusion rates.
Treatment: O_2O_2O2/CO2O_2$$, Beta 1 & 2 Rx.
Prognosis: potentially reversible, but may lead to respiratory failure.
RLD – Tuberculosis (TB)
Was once leading cause of death in U.S.
Still one of top causes of death in world.
15,000 new cases annually in US (250-300 in Alabama).
Caused by infection with Mycobacterium tuberculosis.
Characterized by granulomas, caseous necrosis, and cavity formation.
Transmission: airborne.
Primary versus secondary infection.
Multi-drug resistant TB.
TB (Continued)
At-risk groups:
Immunocompromised
Crowded living conditions
TB Transmission
Primary TB: inhalation of Mycobacterium tuberculosis from infected (Secondary TB).
+ TB skin test denotes exposure.
Body forms Ghon foci calcification around MTB.
Time bomb? May choose to tx with INH x 1 year.
Secondary (post-Primary or Reactivation):
Not due to exogenous infection, rather reinfection of endogenous TB.
TB treatable but difficult to recognize.
Symptoms subtle, easy to ignore, nonspecific (eg, cough, phlegm production, weight loss, dyspnea, night sweats, fever, malaise, anorexia).
Diagnosis: H&P, TB skin test, chest radiograph, microscopic examination and culture of sputum.
During Secondary Infection, person is extremely contagious and should be placed in respiratory isolation until after 10-14 days of anti-TB Rx.
Pharmacologic tx:
Agents that inhibit bacterial protein synthesis on DNR/RNA (INH, rifampin, pyrazinamide).
Agents that inhibit bacterial DNA/RNA synthesis and function (eg, ethambutol, rifampin).
Recommended duration: 6-9 months.
Rx side effects may include liver damage, hepatitis, temporary blindness (optic nerve toxicity), temporary loss of hearing.
RESPIRATORY ISOLATION (mask only).
RLD: Aspiration Pneumonia
Aspiration: inhalation of foreign material, usually food, drink, or vomit; common sequelae of stroke, seizure.
Aspiration pneumonia: inflammation of lungs that results from aspiration.
Introduction of aerobic and anaerobic bacteria into lungs, difficult to treat/resolve.
RLD: Acute Respiratory Distress Syndrome (ARDS)
Acute respiratory failure due to systemic or pulmonary insult (eg, sepsis, trauma, major surgery).
Also called adult respiratory distress syndrome, shock lung, hyaline membrane disease (adult or newborn), diffuse alveolar damage.
Often fatal (80% mortality rate for patients >35 yrs and 20% fatal for patients <35 yrs).
Pathogenesis: damage to alveolar epithelium and capillary endothelium→ pulmonary edema → “drowning” at cellular level.
Onset: within 12-48 hrs, w/ initial presentation of ↑ RR (shallow, rapid).
Characterized by dropping SaO2 while increasing FIO2
Neonates benefit from surfactant replacement Rx
Adults do not benefit from surfactant Rx