Tissues Living Communities Lecture Part 2 Study Notes
Cardiac Muscles and Healing Phases
Comparison of Cardiac Muscles and Skeletal Muscles
Cardiac muscles are unique compared to skeletal muscles in several key aspects.
Skeletal Muscle:
Also known as striated muscle due to the organized arrangement of actin and myosin filaments into sarcomeres.
Characterized as being voluntary, meaning its contractions are consciously controlled by the central nervous system through motor neurons.
Composed of long, cylindrical, multinucleated cells (fibers) that form parallel bundles.
Exhibits visible stripes (striations) under a microscope.
Cardiac Muscle:
Also striated, containing organized sarcomeres, but differs considerably from skeletal muscle.
Involuntary, meaning its contractions are not consciously controlled and are instead regulated by the autonomic nervous system and intrinsic pacemaker cells.
Composed of branched cells, typically containing one or two nuclei, interconnected by specialized junctions.
Contains intercalated discs, which are unique, complex structures found only in cardiac muscle.
These discs contain gap junctions, which allow for rapid electrical impulse conduction from one cardiac cell to the next, enabling the heart to function as a functional syncytium.
They also contain desmosomes, providing strong adhesion between cells, preventing separation during rhythmic contractions.
The presence of intercalated discs is a definitive identifying feature of cardiac muscle in microscopic examinations and is essential for its coordinated pumping action.
Phases of Healing
Understanding the healing process, a complex biological cascade, is crucial for technicians involved in patient care during trauma and surgeries. This process encompasses sequential and overlapping phases.
Phase 1: Inflammation
Begins acutely within 5 to 10 minutes after an injury, serving as the body's immediate protective response to tissue damage.
Characterized by two critical vascular events:
Vasoconstriction:
Immediate and transient (lasting minutes) constriction of damaged blood vessels.
Mediated by neural reflexes and local vasoactive substances (e.g., serotonin, thromboxane).
Primary function is to minimize initial blood loss (hemostasis).
Vasodilation:
Follows vasoconstriction and is more sustained, leading to the widening of local blood vessels.
Increases blood flow to the injured area, bringing essential immune cells and nutrients.
The release of potent mediators is central to this phase:
Histamine and Heparin are released from mast cells located in connective tissues.
Histamine stimulates profound vasodilation and significantly increases capillary permeability, allowing fluid and proteins to leak into the interstitial space.
Heparin acts as an anticoagulant, preventing excessive clotting within the wound, which facilitates the migration of immune cells.
Other inflammatory mediators, such as prostaglandins (contributing to pain and vasodilation) and bradykinin (causing pain, vasodilation, and increased vascular permeability), are also released.
Consequences and clinical signs of inflammation include:
Edema: Swelling due to fluid accumulation in the interstitial space. Initially, it's a transudate (low protein), then transitions to an exudate (high protein, inflammatory cells).
Diapedesis and Phagocytosis:
Diapedesis is the process where white blood cells (leukocytes), primarily neutrophils initially (in acute inflammation) followed by macrophages, migrate from blood vessels into the injured tissue.
Phagocytosis is the process by which these migrated cells (neutrophils and macrophages) engulf and digest pathogens, cellular debris, and foreign tissue, cleaning the wound site.
Heat and Redness: Increased blood flow (hyperemia) to the area leads to these characteristic clinical signs (calor and rubor).
Pain (Dolor): Caused by the release of chemical mediators (e.g., bradykinin, prostaglandins) and the pressure of edema on nerve endings.
Loss of Function (Functio Laesa): A result of pain and swelling, hindering normal movement or activity of the affected area. These five are the cardinal signs of inflammation.
Enhanced supply of oxygen and nutrients is delivered to damaged tissue, crucial for subsequent repair.
Phase 2: Organization
Commences shortly after injury and overlaps significantly with the inflammatory phase.
Phagocytosis continues vigorously, primarily by macrophages, which are essential for thorough debridement and removal of dead tissue, preparing the wound bed for repair.
Formation of Granulation Tissue:
This pivotal tissue forms the foundation for new tissue growth and appears as a soft, pink, bumpy, and highly vascularized tissue.
It is composed of a dense network of new capillaries (formed via angiogenesis) and fibroblasts that synthesize and deposit an extracellular matrix, primarily Type III collagen initially, along with ground substance.
Angiogenesis: The formation of new blood vessels from pre-existing ones is crucial for delivering oxygen and nutrients to the healing tissue and removing waste products. This process is stimulated by hypoxia and various growth factors (e.g., VEGF).
Serves as a provisional framework for the migration and proliferation of other cells involved in healing.
Proud Flesh (Exuberant Granulocytosis):
A pathological condition where granulation tissue formation is excessive, growing above the level of the skin margin. It stems from an overly vigorous and prolonged inflammatory response.
Commonly observed in horses, it can impede epithelialization and delay wound closure, often requiring surgical debridement or topical treatments.
Fluid from plasma continues to fill the affected area, contributing to persistent swelling, which can irritate nerve endings, resulting in pain and tenderness.
Formation of clots is vital; the initial clot helps isolate the area, forming a physical barrier against bacterial invasion.
Clot Formation Process:
Platelets rapidly adhere to exposed collagen at the site of blood vessel injury, become activated and sticky, and aggregate to form a primary plug.
The coagulation cascade is activated, leading to the conversion of soluble fibrinogen into insoluble fibrin strands by the enzyme thrombin.
This fibrin forms a robust meshwork that traps red blood cells and additional platelets, creating a stable fibrin matrix that reinforces the initial platelet plug and provides a provisional scaffold for invading cells.
Phase 3: Regeneration
This phase occurs concurrently with the organization phase, focusing on tissue restoration and remodeling.
Involves Epithelialization:
Basal epithelial cells at the wound edges begin to multiply and migrate across the granulation tissue, forming a new protective layer.
This migration continues until cells from opposite sides meet, at which point contact inhibition stops further movement.
Subsequently, these cells stratify to reform a multi-layered epidermis.
Fibroblasts continue to manufacture abundant collagen (initially Type III, later remodeled to stronger Type I) and ground substance (e.g., proteoglycans, hyaluronic acid) to replace lost or damaged tissue.
Myofibroblasts, specialized fibroblasts with contractile properties, emerge in the wound.
Their contraction is critical for wound contraction, pulling the wound edges closer together, significantly reducing the size of larger open wounds.
As healing progresses, the highly vascularized granulation tissue gradually transforms into less vascular and more fibrous scar tissue.
Complete epithelialization may lead to scab detachment when the underlying new epidermis is fully formed and no longer needs protection.
Scar tissue may form, which is predominantly made of dense Type I collagen fibers, organized differently from original tissue. It is generally less elastic, less vascular, and lacks specialized structures like hair follicles or sweat glands.
Attention to Adhesions:
Adhesions are bands of fibrous scar tissue that form between internal organs or tissues that are normally separate, particularly common after abdominal trauma or surgery.
These can lead to significant complications such as chronic pain, organ dysfunction (e.g., intestinal obstruction, infertility), and can be challenging to manage.
Classifications of Wound Healing
First Intention (Primary Intention) Wounds:
Occur in wounds with clean, sharply incised edges that are brought into close apposition, most typically seen in surgical incisions.
Involves minimal tissue loss and very little inflammation.
Healing occurs rapidly with minimal granulation tissue formation and results in a fine, linear scar.
Second Intention (Secondary Intention) Wounds:
Commonly seen in wounds with significant tissue loss, irregular or separated wound edges, or those that are contaminated, preventing primary closure (e.g., large lacerations, burns, pressure ulcers).
The healing process involves more extensive inflammation, significant granulation tissue formation, and prominent wound contraction.
Takes a longer time to heal and results in a more prominent, often disfiguring, scar.
Third Intention (Delayed Primary Closure):
Applies to wounds that are initially left open for several days (e.g., due to heavy contamination, infection, or extensive edema).
After a period during which the wound is managed (cleaned, debrided, infection controlled), it is then surgically closed when the risk of infection significantly decreases.
This method combines aspects of both first and second intention healing, leading to a scar that is typically more significant than first intention but less so than a full second intention wound.
Conclusion
Understanding tissues, their unique characteristics, and their intricate healing processes is fundamental in both medical and veterinary applications, enabling informed clinical decisions.
Review these detailed notes, and do not hesitate to reach out for more in-depth discussions or clarification if needed.