Division 1Introduction to AdvancedPrehospital Care : Division 1Introduction to AdvancedPrehospital Care
Chapter 4General Principles of PathophysiologyPart I How Normal Body Processes Are Altered by Disease and Injury : Chapter 4General Principles of PathophysiologyPart I How Normal Body Processes Are Altered by Disease and Injury
Topics : Topics Disease Risk
Hypoperfusion
Shock
Multiple Organ Dysfunction Syndrome
Pathophysiology : Pathophysiology The study of how diseases alter the normal physiological processes of the human body
From the root “patho” meaning disease
How Cells Respond to Change and Injury : How Cells Respond to Change and Injury
Cellular Adaptation : Cellular Adaptation Cells, tissues, organs, and organ systems can adapt to both normal and injurious conditions.
Adaptation to external stressors results in alteration of structure and function.
Examples: Growth of the uterus during pregnancy, dilation of the left ventricle after an MI.
Types of Cellular Adaptations(1 of 2) : Types of Cellular Adaptations(1 of 2) Atrophy
Decreased size resulting from a decreased workload
Hypertrophy
An increase in cell size resulting from an increased workload
Types of Cellular Adaptations(2 of 2) : Types of Cellular Adaptations(2 of 2) Hyperplasia
An increase in the number of cells resulting from an increased workload
Metaplasia
Replacement of one type of cell by another type of cell that is not normal for that tissue
Dysplasia
A change in cell size, shape, or appearance caused by an external stressor
Cellular Injury : Cellular Injury Hypoxic
Chemical
Infectious
Immunologic/Inflammatory
Physical agents
Nutritional balances
Genetic factors
Manifestation of Cellular Injury : Manifestation of Cellular Injury When cells are injured metabolism is changed, causing substances to infiltrate or accumulate to an abnormal degree in cells.
Cellular Swelling : Cellular Swelling Results from a permeable or damaged cellular membrane
Caused by an inability to maintain stable intra- and extracellular fluid and electrolyte levels
Fatty Change : Fatty Change Lipids invade the area of injury.
Occurs most commonly in vascular organs, most frequently the liver.
Causes a disruption of the cellular membrane and metabolism and interferes with the vital functions of the organ.
Signs and Symptoms of Cellular Change : Signs and Symptoms of Cellular Change Fatigue and malaise
Altered appetite
Fever
Increased heart rate associated with fever
Pain
Cell Death (1 of 3) : Cell Death (1 of 3) Apoptosis
Injured cell releases enzymes that engulf and destroy the cell.
Cells shrink.
Eliminating damaged and dead cells allows tissues to repair and possibly regenerate.
Cell Death (2 of 3) : Cell Death (2 of 3) Necrosis
A pathological process
Cells swell and rupture
Coagulative
Liquefactive
Caseous
Fatty
Cell Death (3 of 3) : Cell Death (3 of 3) Gangrenous necrosis
Cell death over a wide area
Dry
Wet
Gas
Fluids and Fluid Imbalances : Fluids and Fluid Imbalances
Slide 18 : Water is the most abundant substance in the human body.
Where the Water Is Found : Where the Water Is Found Intracellular fluid—fluid inside the cells
Extracellular fluid—all the fluid outside the body cells
Intravascular fluid—fluid within the circulatory system
Interstitial fluid—fluid outside of the cell membranes but not within the circulatory system
Edema : Edema Accumulation of water in the interstitial space due to disruption in the forces and mechanisms that normally keep net filtration at zero
Mechanisms That Cause Edema : Mechanisms That Cause Edema A decrease in plasma oncotic force
An increase in hydrostatic pressure
Increased capillary permeability
Lymphatic channel obstruction
Edema (1 of 2) : Edema (1 of 2) Can be local or within a certain organ system
Sprained ankle vs. pulmonary edema
Edema (2 of 2) : Edema (2 of 2) Water in interstitial spaces is not available for metabolic processes.
Edema, therefore, can cause a relative condition of dehydration.
Intravenous Therapy : Intravenous Therapy
Slide 25 : Blood Components
Slide 26 : The percentage of the blood occupied by the red blood cells is termed the hematocrit.
Fluid Replacement : Fluid Replacement
Slide 28 : Transfusion reactions occur when there is a discrepancy between the blood type of the patient and the type of the blood being transfused. Transfusion Reactions
Signs and Symptoms of Transfusion Reactions : Signs and Symptoms of Transfusion Reactions Fever
Chills
Hives
Hypotension
Palpitations
Tachycardia Flushing of the skin
Headache
Loss ofconsciousness
Nausea
Vomiting
Shortness of breath
Treatment of Transfusion Reactions (1 of 2) : Treatment of Transfusion Reactions (1 of 2) IMMEDIATELY stop the transfusion.
Save the substance being transfused.
Rapid IV infusion.
Treatment of Transfusion Reactions (2 of 2) : Treatment of Transfusion Reactions (2 of 2) Assess the patient’s mental status.
Administer oxygen.
Contact medical direction.
Be prepared to administer mannitol, diphenhydramine, or furosemide.
Intravenous Fluids : Intravenous Fluids
Hemoglobin-Based Oxygen-Carrying Solutions (HBOCs) : Hemoglobin-Based Oxygen-Carrying Solutions (HBOCs) Commonly referred to as “blood substitutes”
Compatible with all blood types
Do not require blood typing, testing, or cross-matching
PolyHeme
Hemopure
Colloids : Colloids Colloids remain in intravascular spaces for an extended period of time and have oncotic force.
Plasma protein fraction (Plasmanate)
Salt-poor albumin
Dextran
Hetastarch (Hespan)
Crystalloids : Crystalloids Crystalloid solutions are the primary compounds used in prehospital care.
Isotonic solutions
Hypertonic solutions
Hypotonic solutions
Slide 36 : The effects of hypertonic,
isotonic, and
hypotonic solutions
on red blood cells
Most Commonly Used Solutions in Prehospital Care : Most Commonly Used Solutions in Prehospital Care
Acid-Base Derangements : Acid-Base Derangements
Respiratory Acidosis : Caused by abnormal retention of CO2 from impaired ventilation due to problems occurring in the lungs or respiratory center of the brain. Respiratory Acidosis
Respiratory Alkalosis : Caused by increased respiration and excessive elimination of CO2. The CO2 level is decreased and the pH is increased. Respiratory Alkalosis
Metabolic Acidosis : Results from the production of metabolic acids such as lactic acid. These acids consume bicarbonate ions.
Can be the result of dehydration, diabetes, or medication usage. Metabolic Acidosis
Slide 42 : Compensation for metabolic acidosis begins with an increase in respirations.
Metabolic Alkalosis : Metabolic Alkalosis The pH is increased and the CO2 level is normal. It is usually caused by administration of diuretics, loss of chloride ions associated with prolonged vomiting, and overzealous administration of sodium bicarbonate.
Slide 44 : Genetics and Other Causes of Disease
Many Factors Combine to Cause Disease (1 of 3) : Many Factors Combine to Cause Disease (1 of 3) Genetics
Environment
Lifestyle
Age
Gender
Many Factors Combine to Cause Disease (2 of 3) : Many Factors Combine to Cause Disease (2 of 3) Inherited traits are determined by molecules of deoxyribonucleic acid (DNA).
Each somatic cell contains 46 chromosomes.
Sex cells contain 23 chromosomes.
Many Factors Combine to Cause Disease (3 of 3) : Many Factors Combine to Cause Disease (3 of 3) An offspring receives 23 chromosomes from the mother and 23 chromosomes from the father.
One or more chromosomes may be abnormal and may cause a congenital disease or a propensity toward acquiring a disease later in life.
Slide 48 : Most disease processes are multifactorial in origin.
Disease Effects on Individuals : Disease Effects on Individuals Host
Agent
Environment
Disease Effects on Populations : Disease Effects on Populations Incidence
Prevalence
Mortality
Family History and Associated Risk Factors : Family History and Associated Risk Factors
Immunologic Disorders : Immunologic Disorders A number of immunologic disorders are more prevalent among those with a family history of the disorder.
Cancer : Cancer Some types of cancer tend to cluster in families and seem to have a combination of genetic and environmental causes.
Breast cancer
Colorectal cancer
Endocrine Disorders : Endocrine Disorders The most common endocrine disorder is diabetes mellitus.
Leading cause of:
Blindness
Heart disease
Kidney failure
Premature death
Both Type I and Type II diabetes can be family related.
Hematological Disorders : Hematological Disorders There are many causes of hereditary hematological disorders such as gene alteration and histocompatibility (tissue interaction) dysfunctions.
Hemophilia
Hemochromatosis
Cardiovascular Disorders : Cardiovascular Disorders The cardiovascular system can be greatly affected by genetic disorders.
Elongation of the QT interval
Mitral valve prolapse
Coronary artery disease
Hypertension
Cardiomyopathy
Renal Disorders : Renal Disorders Caused by a variety of factors, primarily hypertension.
EMS is increasingly being called upon to deal with complications of dialysis including:
Problems with vascular access devices
Localized infection and sepsis
Electrolyte imbalances
Rheumatic Disorders : Rheumatic Disorders Gout is a disorder both genetic and environmental characterized by the deposit of crystals in the joints, most commonly the great toe.
The crystals form as a result of abnormally high levels of uric acid in the blood.
Gastrointestinal Disorders : Gastrointestinal Disorders Lactose intolerance
Crohn’s disease
Peptic ulcers
Cholecystitis
Obesity
Neuromuscular Disorders : Neuromuscular Disorders Diseases of the nervous and muscular systems include:
Huntington’s disease
Multiple sclerosis
Alzheimer’s disease
Psychiatric Disorders : Psychiatric Disorders Genetic and biological causes of these disorders are being studied and increasingly understood.
Schizophrenia
Manic-depressive illness (bipolar disorder)
Hypoperfusion : Hypoperfusion
Slide 63 : Hypoperfusion (shock) is inadequate perfusion of body tissues.
Slide 64 : Progression of Shock
The Pathophysiology of Hypoperfusion : The Pathophysiology of Hypoperfusion
Causes of Hypoperfusion (1 of 3) : Causes of Hypoperfusion (1 of 3) Inadequate pump
Inadequate preload
Inadequate cardiac contractile strength
Excessive afterload
Causes of Hypoperfusion (2 of 3) : Causes of Hypoperfusion (2 of 3) Inadequate fluid
Hypovolemia
Causes of Hypoperfusion (3 of 3) : Causes of Hypoperfusion (3 of 3) Inadequate container
Dilated container without change in fluid volume (inadequate systemic vascular resistance)
Leak in the container
Shock at the Cellular Level : Shock at the Cellular Level Shock causes vary; however, the ultimate outcome is impairment of cellular metabolism.
Impaired Use of Oxygen : Impaired Use of Oxygen When cells don’t receive enough oxygen or cannot use it effectively, they change from aerobic to anaerobic metabolism.
Glucose Breakdown (1 of 2) : Glucose Breakdown (1 of 2) Stage one, glycolysis, is anaerobic (does not require oxygen). It yields pyruvic acid, with toxic by-products such as lactic acid, and very little energy.
Glucose Breakdown (2 of 2) : Stage two is aerobic (requires oxygen). In a process called the Krebs or citric acid cycle, pyruvic acid is degraded into carbon dioxide and water, which produces a much higher yield of energy. Glucose Breakdown (2 of 2)
Compensation and Decompensation : Compensation and Decompensation Usually the body is able to compensate for any changes. However, when the various compensatory mechanisms fail, shock develops and may progress.
Compensation Mechanisms : Compensation Mechanisms The catecholamines epinephrine and norepinephrine may be secreted.
The renin-angiotensin system aids in maintaining blood pressure.
Another endocrine response by the pituitary gland results in the secretion of anti-diuretic hormone (ADH).
Shock Variations (1 of 3) : Shock Variations (1 of 3) Compensated shock is the early stage of shock during which the body’s compensatory mechanisms are able to maintain normal perfusion.
Shock Variations (2 of 3) : Shock Variations (2 of 3) Decompensated shock is an advanced stage of shock that occurs when the body’s compensatory mechanisms no longer maintain normal perfusion.
Shock Variations (3 of 3) : Shock Variations (3 of 3) Irreversible shock is shock that has progressed so far that the body and medical intervention cannot correct it.
Types of Shock : Types of Shock Cardiogenic
Hypovolemic
Neurogenic
Anaphylactic
Septic
Cardiogenic Shock : Cardiogenic Shock The heart loses its ability to supply all body parts with blood.
Usually the result of left ventricular failure secondary to acute myocardial infarction or CHF.
Many patients will have normal blood pressures.
Cardiogenic Shock Evaluation : Cardiogenic Shock Evaluation The major difference between cardiogenic shock and other types of shock is the presence of pulmonary edema causing:
Difficulty breathing.
As fluid levels rise, wheezes or crackles (rales) may be heard.
There may be a productive cough with white or pink-tinged foamy sputum.
Cyanosis, altered mentation, and oliguria.
Cardiogenic Shock Treatment (1 of 2) : Cardiogenic Shock Treatment (1 of 2) Assure an open airway.
Administer oxygen.
Assist ventilations as necessary.
Keep the patient warm.
Cardiogenic Shock Treatment (2 of 2) : Cardiogenic Shock Treatment (2 of 2) Elevate the patient’s head and shoulders.
Establish IV access with minimal fluid administration.
Monitor the heart rate.
Dopamine or dobutamine may be administered.
Hypovolemic Shock : Hypovolemic Shock Shock due to loss of intravascular fluid
Internal or external hemorrhage
Trauma
Long bones or open fractures
Dehydration
Plasma loss from burns
Excessive sweating
Diabetic ketoacidosis with resultant osmotic diuresis
Hypovolemic Shock Evaluation (1 of 2) : Hypovolemic Shock Evaluation (1 of 2) Altered level of consciousness.
Pale, cool, clammy skin.
Blood pressure may be normal, then fall.
Hypovolemic Shock Evaluation (2 of 2) : Hypovolemic Shock Evaluation (2 of 2) Pulse may be normal then become rapid, finally slowing and disappearing.
Urination decreases.
Cardiac dysrhythmias may occur.
Hypovolemic Shock Treatment : Hypovolemic Shock Treatment Airway control.
Control severe bleeding.
Keep the patient warm.
Administer a bolus of crystalloid solution for fluid replacement.
Non-trauma or no blood loss:
Bolus crystalloid or colloid solutions
Trauma or blood loss:
“Permissive hypotension” – SBP of 70-85 mmHg
PASG if part of local protocol.
Neurogenic Shock : Neurogenic Shock Results from injury to brain or spinal cord causing an interruption of nerve impulses to the arteries.
The arteries dilate causing relative hypovolemia.
Sympathetic impulses to the adrenal glands are lost, preventing the release of catecholamines with their compensatory effects.
Neurogenic Shock Evaluation : Neurogenic Shock Evaluation Warm, dry, red skin
Low blood pressure
Slow pulse
Neurogenic Shock Treatment : Neurogenic Shock Treatment Airway control.
Maintain body temperature.
Immobilization of patient.
Consider other possible causes of shock.
IV access and medications that increase peripheral vascular resistance.
Anaphylactic Shock : Anaphylactic Shock A severe immune response to a foreign substance.
Signs and symptoms most often occur within a minute, but can take up to an hour.
The most rapid reactions are in response to injected substances:
Penicillin injections
Bees, wasps, hornets
Anaphylactic Shock Evaluation : Anaphylactic Shock Evaluation Cardiovascular system:
Vasodilation, increased heart rate, decreased blood pressure
Gastrointestinal system:
Nausea, vomiting, abdominal cramping, diarrhea
Nervous system:
Altered mental status, dizziness, headache, seizures, tearing
Anaphylactic Shock Treatment : Anaphylactic Shock Treatment Airway protection; may includeendotracheal intubation.
Establish an IV of crystalloidsolution.
Pharmacological intervention:
Epinephrine, antihistamines, corticosteroids, vasopressors, inhaled beta agonists
Septic Shock : Septic Shock An infection that enters the bloodstream and is carried throughout the body.
The toxins released overcome the compensatory mechanisms.
Can cause the dysfunction of an organ system or result in multiple organ dysfunction syndrome.
Septic Shock Evaluation : Septic Shock Evaluation The signs and symptoms are progressive.
Increased to low blood pressure
High fever, no fever, or hypothermic
Skin flushed, pale, or cyanotic
Difficulty breathing and altered lung sounds
Altered mental status
Septic Shock Treatment : Septic Shock Treatment Airway control.
IV of crystalloid solution.
Dopamine to support blood pressure.
Monitor heart rhythm.
Multiple Organ Dysfunction Syndrome : Multiple Organ Dysfunction Syndrome MODS is the progressive impairment of two or more organ systems from an uncontrolled inflammatory response to a severe illness or injury.
Slide 97 : MODS Stages
Primary MODS : Primary MODS Organ damage results directly from a specific cause such as ischemia or inadequate tissue perfusion from shock, trauma, or major surgery.
Stress and inflammatory responses may be mild and undetectable.
During this response, neutrophils, macrophages, and mast cells are thought to be “primed” by cytokines.
Secondary MODS : Secondary MODS The next time there is an injury, ischemia, or infection, the “primed” cells are activated, producing an exaggerated inflammatory response.
The inflammatory response enters a self-perpetuating cycle causing damage and vasodilation.
An exaggerated neuroendocrine response is triggered causing further damage.
MODS 24 Hours after Resuscitation : MODS 24 Hours after Resuscitation Low grade fever
Tachycardia
Dyspnea
Altered mental status
General hypermetabolic, hyperdynamic state
MODS within 24 to 72 Hours : MODS within 24 to 72 Hours Pulmonary failure begins.
MODS within 7 to 10 Days : MODS within 7 to 10 Days Hepatic failure begins.
Intestinal failure begins.
Renal failure begins.
MODS within 14 to 21 Days : MODS within 14 to 21 Days Renal and hepatic failure intensify.
Gastrointestinal collapse.
Immune system collapse.
MODS after 21 Days : MODS after 21 Days Hematological failure begins.
Myocardial failure begins.
Altered mental status resulting from encephalopathy.
Death.
Summary : Summary Disease Risk
Hypoperfusion
Shock
Multiple Organ Dysfunction Syndrome