Alexander ch10 lecture

Copyright © 2017, 2012 Pearson Education, Inc. All Rights Reserved.
Advanced EMT
A Clinical-Reasoning Approach, 2nd Edition
Chapter 10
Pathophysiology:
Selected Impairments
of Homeostasis

• The Advanced EMT applies comprehensive
knowledge of the pathophysiology of respiration
and perfusion to patient assessment and
management.
Advanced EMT
Education Standard

1. Define key terms introduced in this chapter.
2. Explain the importance of understanding basic
pathophysiology.
3. Give examples of mechanisms that cause disease and
injury in the human body.
4. Describe the composition of ambient air as it relates to
ventilation and respiration.
5. Explain how changes in the compliance of the lungs and
chest wall and in airway resistance can affect ventilation.
Objectives (1 of 6)

6. Explain how common disease processes can interfere
with ventilation and with external and internal respiration.
7. Describe the homeostatic mechanisms that attempt to
correct for changes in ventilation and perfusion.
8. Explain the consequences of impaired tidal volume,
respiratory rate, and minute volume, as well as increases
in anatomical dead space.
9. Explain the concept of ventilation–perfusion mismatch.
10.Explain the pathophysiology of shock (hypoperfusion),
including the consequences of cellular hypoxia and
death.
Objectives (2 of 6)

11.Compare and contrast aerobic and anaerobic cellular
metabolism, including consideration of the amount of ATP
produced and the removal of byproducts of energy
metabolism.
12.Describe the consequences of failure of the cellular
sodium/potassium pump.
13.Describe how inadequate vascular volume, inadequate
heart function, and decreased peripheral vascular
resistance can each lead to shock.
Objectives (3 of 6)

14.Give examples of conditions that can lead to loss of
vascular volume, inadequate heart function, and
decreased peripheral vascular resistance.
15.Explain the mechanisms and pathophysiology of each of
the following types of shock: hypovolemic (hemorrhagic
and nonhemorrhagic), distributive (anaphylactic, septic,
neurogenic), cardiogenic, and obstructive.
16.Explain how mechanisms such as exposure to carbon
monoxide and cyanide can lead to shock.
Objectives (4 of 6)

17.Explain the body’s compensatory reactions to
hypoperfusion and how they manifest in the early signs
and symptoms of shock.
18.Describe the progression of shock through the
compensated, decompensated, and irreversible stages.
19.Discuss the rationales behind the priorities and goals of
prehospital management of patients with hypoperfusion.
20.Given a series of scenarios, recognize patients who are
at risk for shock and explain the influence of age on the
assessment and management of patients with
hypoperfusion.
Objectives (5 of 6)

21.Describe the pathophysiology of cardiac arrest.
22.Differentiate among the electrical, circulatory, and
metabolic phases of cardiac arrest.
23.Explain the dependence of cells upon glucose as a
source of energy.
24.Explain the consequences of untreated hypoglycemia.
25.Explain how disruptions of electrolyte balance and pH
affect body functions.
26.Explain the consequences of inadequate temperature
regulation in the body.
Objectives (6 of 6)

• Homeostasis
– a physiologic steady state achieved by the body’s
complex regulatory mechanisms.
• When disease, environmental conditions, or
trauma disrupts homeostasis, the body responds,
correcting the disruption.
Introduction (1 of 3)

• Body’s compensatory mechanisms respond, but
they are not sufficient.
• Signs and symptoms appear, but they are
superficial indications.
• AEMT must recognize signs and symptoms, and
understand what causes them.

• Physiology
• Pathology
• Pathophysiology
• All diseases and injuries affect the body at cellular
level.
• Body responds in predictable ways to specific
threats to homeostasis.

• What problems require immediate attention?
• What are potential underlying causes of the
problems?
• How can looking for underlying causes of the
problems be important in making decisions about
treatment?
Think About It

• Mechanisms of homeostasis can be disrupted
– Hypoxia
– Nutritional imbalance
– Genetic diseases
– Cancer
– Physical injury
– Toxins
– Infections
Mechanisms of Disease and Injury (1 of
2)

Table 10-1 (1 of 2)
Selected Mechanisms of Disease
Disease Mechanism Example Pathophysiology
Hypoxia A narcotic overdose
depresses the respiratory
centers in the central
nervous system.
Decreased respiratory center function causes slow, shallow
ventilations. An inadequate amount of air reaches the alveolar
level for gas exchange, resulting in poor oxygenation of the
blood returning to the lungs. Inadequately oxygenated red
blood cells cannot deliver sufficient oxygen at the cellular level.
Without oxygen, the cells engage in anaerobic metabolism,
producing less ATP. Without ATP, cellular mechanisms fail, and
cell death occurs.
Nutritional imbalance A patient with diabetes
takes insulin but does not
eat.
The increased amount of insulin quickly facilitates the entry of
the available glucose into cells. Without an additional source
of glucose from the digestive tract, the blood glucose level
quickly falls. The remaining glucose is inadequate to fuel the
metabolic needs of the cell. ATP is not produced, and cellular
mechanisms begin to fail.
Physical trauma A patient falls from a
second-story roof. When he
lands, a screwdriver in his
tool belt impales him in the
right side, lacerating his
liver. The liver begins to
bleed profusely.
With a decreased number of red blood cells, inadequate
oxygen and glucose are delivered to the cells to fuel
metabolism, and cellular mechanisms begin to fail. Unless the
bleeding is stopped quickly and red blood cells are restored,
the patient will die.

Table 10-1 (2 of 2)
Selected Mechanisms of Disease
Disease Mechanism Example Pathophysiology
Infection A patient develops
pneumonia.
Cellular debris and fluid fill the alveoli in the affected lobe,
preventing oxygen from diffusing across the respiratory
membrane and into the blood. Less oxygen reaches the
cellular level, impairing cellular metabolism.
Toxin A faulty gas furnace
releases carbon monoxide
into a residence.
Carbon monoxide binds to hemoglobin, preventing oxygen
from binding to it. Oxygen is not delivered to the cellular level,
impairing cellular metabolism.
Environment A person locks his keys in
his car and is unable to get
back into his car or into his
house. It is 2 degrees
Fahrenheit with a 20-mph
wind. His closest neighbor
is three miles away.
The body loses heat to the cold air, and this effect is increased
substantially by the wind. Despite shivering and the exercise
of walking to get help, the body is unable to generate enough
heat to maintain the core temperature. The electrical system
of the heart becomes irritable, the nervous system begins to
malfunction, and less oxygen is released to the cells in the
tissues.

Mechanisms of Disease and Injury (2 of
2)
• Category of mechanisms
– Hypoxic cellular injury
– Shock
– Impaired glucose metabolism
– Electrolyte and pH disturbance
– Environmental disorders
• Considerable overlap among mechanisms

• Body capable of remarkable adaptation under
stress.
– withstand significant challenges to homeostasis.
• Long term, cells adapt to variety of conditions.
Compensation and Adaptation

Table 10-2
Types of Cellular Adaptation
Adaptation Description
Atrophy Reduction in the size of cells of a tissue. For example, skeletal muscle atrophy occurs when an
extremity has been immobilized in a cast for several weeks. Cells adapt to the lack of use by
decreasing in size.
Metaplasia A change in the type of cells that comprise a tissue into a different type of cell that is not normal for
that tissue in order to adapt to changes in the environment. For example, cells that line the
esophagus (squamous epithelium) can change into a different type (columnar epithelium) to adapt
to chronic exposure to stomach acids (Barrett’s esophagus).
Hyperplasia Increase in the number of cells of a tissue. An example is benign prostatic hypertrophy in middle-
age men. The prostate increases in size and can obstruct the urethra, interfering with urine flow.
Hypertrophy Increase in the size of cells of a tissue. The best example of this is the growth of a muscle following
weight lifting. The number of skeletal muscle cells remains constant, but cell size increases.
Anaplasia Loss of cellular differentiation. This is an indication of malignant tumors.
Dysplasia Cell maturation and differentiation are delayed, resulting in the loss of uniformity of cells within a
certain tissue. This is often a precursor to cancer. For example, a Pap smear may show dysplasia
of cells of the cervix, indicating a need for further examination and treatment to prevent cancer.
Neoplasia New or expanded growth in an area of the body where it is not expected. Neoplasia can be
accompanied by anaplasia. This, and the degree to which the neoplasm invades normal tissues,
determines whether or not the tumor is benign or malignant. An example of a benign neoplasm is
uterine fibroid tumors. An example of a malignant neoplasm is osteosarcoma, a cancerous bone
tumor.
Apoptosis The genetic instructions provided by DNA can command cellular self-destruction, either as part of a
normal process or to destroy damaged cells that are a threat to the body.

Figure 10-2 (1 of 2)
(A) Aerobic metabolism. Glucose broken down in the presence of oxygen produces a large
amount of energy (ATP).

Figure 10-2 (2 of 2)
(B) Anaerobic metabolism. Glucose broken down without the presence of oxygen produces
pyruvic acid, which converts to lactic acid and only a small amount of energy (ATP).

Hypoxic Cellular Injury (1 of 15)
• Ischemia
– lack of blood flow to tissues resulting in hypoxia
• Can be reversed by
– restoring perfusion
– adequate ventilation and supplemental oxygen
• Cells initially adapt by switching from aerobic to
anaerobic metabolism
– Only lasts for a limited time (as little as 5 minutes)

• Hypoxic cellular injury
– occurs any time oxygen to cells is disrupted.
• Oxygen required to produce energy
– ATP that fuels cellular work.
• Without ATP
– cells cannot power their reactions and activities.

• Aerobic metabolism is the breakdown of oxygen
and glucose to produce a large amount of energy.
• Anaerobic respiration is the mechanism to
produce ATP without oxygen.
– Short-term adaptation

Figure 10-4
(A) Alveolar/capillary gas exchange. Oxygen moves from the lung alveolus into the
capillary. Carbon dioxide moves from the capillary into the lung. (B) Capillary/cell gas
exchange. Oxygen and nutrients move from the capillary into the cell. Carbon dioxide and
other wastes move from the cell into the capillary.

• Needed for adequate oxygen delivery
– Adequate onloading of oxygen onto hemoglobin in red
blood cells.
– Circulation of red blood cells through microvasculature
to perfuse tissues of the body.
– Adequate offloading of oxygen to tissues once red
blood cells reach microvasculature.

• Components disrupted in four ways
– Oxygen delivery to bloodstream
– Oxygen transport within bloodstream
– Oxygen transport from bloodstream to cells
– Oxygen utilization by cells

• Oxygen delivery to the blood
– The air we breathe contains 21% oxygen; 79%
nitrogen; trace gases.
– Ventilations must produce adequate tidal and minute
volume to provide oxygen.
– Body compensates for decreased tidal volume by
increasing respiratory rate.

• Oxygen delivery to the blood (continued)
– Shallow breathing results in inadequate ventilation.
– Atmospheric pressure and partial pressure of oxygen
decrease at high altitudes.
– Symptoms of altitude sickness can develop at
elevations over 8,000 feet.

• Airway must be unobstructed for oxygen to reach
the alveoli.
• Causes
– Swelling from infection
– Allergic reaction
– Trauma
– Relaxation of tongue and throat muscles
– Foreign bodies lodged in airway

Figure 10-5
Nervous control of respiration.

• Respiratory centers in brain must function to
stimulate inspiration and respiratory cycle.
• Anything that blocks communication between the
nervous and respiratory system can lead to
hypoxia.

• Alveoli must be close to the capillaries for oxygen
to diffuse.
– Pulmonary edema, pneumonia
• Bronchoconstriction
– Asthma, COPD, and anaphylaxis result in constriction
of bronchioles.
• Surfactant
– Keep the alveoli from collapsing

• Ventilation-perfusion (VQ) mismatch; decrease in
ventilation, lung perfusion, or both.
– If underlying problem not corrected, respiratory failure
occurs.
– Untreated, respiratory failure leads rapidly to
respiratory arrest.
– Untreated respiratory arrest leads to cardiac arrest
and death.

• Oxygen transport in the blood
– Anemia
 Number of red blood cells decreased with accompanying
decrease in hemoglobin; reduced oxygen carrying capacity.
– Acidosis and alkalosis alter ability of oxygen to bind
with, and release from, hemoglobin.

• Oxygen transport in the blood (continued)
– Cardiac arrest
 Heart stops beating, oxygen delivery to cells cease
– Define each of the following terms
 CPR
 SCA
 Defibrillation

• AHA chain of survival
– Immediate recognition of cardiac arrest and EMS
notification
– Immediate CPR with emphasis on chest compressions
– Rapid defibrillation
– Early advanced life support
– Integrated postresuscitation management

• Alkalotic states cause a diminished ability of
hemoglobin to deliver oxygen to tissues that
need it.
• Cyanide is the substance that prevents cell from
using oxygen.
– Aerobic metabolism cannot occur; cells switch to
anaerobic metabolism.
– If untreated, cyanide poisoning rapidly causes death
from asphyxia.

• Through glycolysis, cells use glucose to produce
ATP.
• Briefly, some cells can adapt to alternative
mechanisms of energy production.
– Not as effective
– Toxic byproducts
Cellular Glucose Use (1 of 3)

• Insulin must be present to facilitate glucose
passage across cell membrane.
• Without insulin, glucose remains in blood.
• Cells uses other sources to create energy.
– Fatty acids
– Ketones
– Diabetic ketoacidosis

• Normal glucose
– 80–120 mg/dL
• Influenced by insulin and glucagon
• Hypoglycemia
– Sympathetic signs and symptoms
– Brain dysfunction

Table 10-3
Signs and Symptoms of Hypoglycemia
 Anxiety
 Sweating
 Tremor
 Extreme hunger
 Rapid heartbeat
 Irritability
 Confusion, difficulty thinking
 Anger
 Weakness
 Blurred vision
 Slurred speech
 Staggering, poor coordination
 Seizures
 Unresponsiveness (coma)

Acid–Base and Electrolyte Disturbances
(1 of 4)
• Causes of acidosis
– Hypoxia
– Diabetic ketoacidosis (DKA)
– Toxicity with acidic substances (aspirin, salicylates, and
antifreeze solutions)
• Metabolic acidosis
– Arterial pH of less than 7.35; bicarbonate level less
than 24 mmHg

(2 of 4)
• As pH decreases, hemoglobin becomes less
effective at binding oxygen.
• Forces cells to utilize anaerobic metabolism;
produces less ATP.
• Hypoxia further worsens acidosis.

(3 of 4)
• Metabolic Alkalosis
– Antacids
– Vomiting
– Diuretics
• Signs and symptoms vary but hypoventilation can
occur in severe cases

(4 of 4)
• Electrolyte abnormalities may be present.
• Electrolytes must be maintained within narrow
ranges for normal cellular function and fluid
balance.
• Cardiac rhythm, electrical conduction, and
contraction can be affected.

Figure 10-10
Progression of inadequate perfusion to cellular death.

Shock (1 of 17)
• All forms of shock share final common pathway of
inadequate cellular perfusion to meet metabolic
needs.
• Shock is inadequate oxygen supply to meet the
demand for oxygen at cellular level.
– What are the four general classifications of shock?

Figure 10-11
Progression of hypovolemic shock.

Shock (2 of 17)
• Hypovolemic shock
– Hypoperfusion from loss of blood volume
 Actual blood loss
 Loss of volume
– Insufficient blood volume within the vascular space
prevents tissues and organs from being perfused

• Hypovolemic shock (continued)
– Compensated shock
– Decompensated shock
– Irreversible shock
– Signs and symptoms
 Classic presentation of shock
 Tachycardia—early sign
 Decreased blood pressure—late sign
Shock (3 of 17)

• Hypovolemic shock—vascular level
– Ischemic phase
– Stagnant phase
– Washout phase
Shock (4 of 17)

• Hemorrhagic shock
– Type of hypovolemic shock.
 Due to blood loss
– Blood loss may not be obvious.
– Chest cavity, abdomen, pelvis, and thigh can hold
enough blood to result in shock.
Shock (5 of 17)

Table 10-4
Stages of Hemorrhagic Shock
Classification of Hemorrhage
Class Blood Volume Loss in 70 kg Adult Signs
Class I hemorrhage Up to 15 percent (750 mL) Usually well tolerated
Can lead to mild tachycardia
Class II hemorrhage 15–30 percent (750–1,500 mL) Moderate tachycardia
Pale skin
Delayed capillary refill
Class III hemorrhage 30–40 percent (1,500–2,000 mL) Tachycardia
Failure of compensation
Hypotension
Class IV hemorrhage 40–50 percent (2,000–2,500 mL) Profound hypotension
End-organ failure (for example, bradycardia,
anuria)
Death

Figure 10-13
Progression of cardiogenic shock.

• Cardiogenic shock
– Heart cannot pump sufficiently enough to maintain
cardiac output.
 Anxiety
 Pale and diaphoretic skin
 Chest pain (if due to myocardial infarction)
 Pulmonary edema
 Fast or slow heart rate
Shock (6 of 17)

• Cardiogenic shock (continued)
– Prehospital treatment
 Supporting airway, breathing, and circulation
– Treatment
 Medications, electrical therapies, interventions to correct
underlying cause
– Mortality rate high
Shock (7 of 17)

Figure 10-14
Progression of neurogenic shock.

• Distributive shock
– Uncontrolled vasodilation, creating vascular container
too large for amount of blood in body
– Three mechanisms of distributive shock
 Neurogenic
 Anaphylactic
 Septic
Shock (8 of 17)

• Neurogenic Shock
– Loss of sympathetic tone results in uncontrolled
vasodilatation below injury site; result can be sudden
onset of hypotension.
– Different signs and symptoms than other types of
shock.
 Skin warm, dry, and pink
 Heart rate normal
 Possible impaired ventilation
Shock (9 of 17)

• Neurogenic Shock (continued)
 Cervical collar and position to manage spinal injury
per protocol
 Airway management; supporting ventilations
 Supplemental oxygen; keep patient warm
 Administer IV fluids according protocol
Shock (10 of 17)

Figure 10-15
Progression of anaphylactic shock.

• Anaphylactic shock
– Result of severe allergic reaction
– Common causes
 Antibiotics, hymenoptera (bee or wasp) stings, and peanuts
Shock (11 of 17)

Shock (12 of 17)
• Anaphylactic shock (continued)
– Can progress quickly, leading to death in minutes
 Hives, itching in throat, stridor, wheezing, abdominal cramping,
and airway swelling
– Treatment
 Epinephrine, IV fluids (per protocol), diphenhydramine (per
protocol)

Figure 10-16
Progression of septic shock.

Shock (13 of 17)
• Septic shock
– Result of systemic inflammatory response to
a pathogen
 high fever (may be absent in elderly), tachycardia, respiratory
distress, decreased mental status, and hypotension.
 Manage airway, ventilation, circulation, and body temperature.

Figure 10-17
Causes of obstructive shock. (A) Pulmonary embolism. (B) Tension pneumothorax. (C)
Pericardial tamponade.

Shock (14 of 17)
• Obstructive shock
– Physical obstruction blocking forward flow of blood
through circulatory system
– Causes
 Pulmonary embolism, tension pneumothorax, and pericardial
tamponade

Shock (15 of 17)
• Pathophysiology of shock
– Regardless of cause, initial signs and symptoms of
shock are external manifestations of the body’s
compensatory reactions to hypoperfusion.
– As shock progresses, signs and symptoms reflect
failure of compensatory mechanisms.

Shock (16 of 17)
• Pathophysiology of shock (continued)
– Many signs and symptoms due to the release of
epinephrine and norepinephrine
 Anxiety
 Pale, cool, sweaty skin
 Tachycardia
 Nausea, vomiting
 Thirst
 Decreased urine output
 Increased respiratory rate

Shock (17 of 17)
• Pathophysiology of shock (continued)
– Your role is to
 Anticipate and recognize shock quickly
 Provide appropriate field interventions
 Provide transportation to the closest facility capable of
providing care the patient needs

Think About It
• Children and geriatric patients do not exhibit the
same signs of shock as an adult.
• How do the signs and symptoms of shock differ
in children?
• How do the signs and symptoms of shock differ in
geriatric patients?

• Body constantly adjusts to changes in internal and
external environment.
• Normal core body temperature 98.6°F (37°C).
• Increased physiologic activity generates heat.
• When core temperature drops, body adjusts to
increase heat production and decrease heat loss.
Heat and Cold Emergencies (1 of 2)

• Shivering uses energy and generates heat.
• When the body cannot compensate for
environmental extremes, or temperature
regulation mechanisms are impaired, death
can occur.
Heat and Cold Emergencies (2 of 2)

Chapter Summary (1 of 2)
• Diseases and injuries often present as
emergencies when pathophysiology results in
inadequate cellular energy production to maintain
cell functions.
• Prehospital treatment
– Ensure delivery of oxygen and glucose to cells;
maintain normal body temperature.

Chapter Summary (2 of 2)
• AEMT provides general, supportive treatments to
maintain patient’s airway, breathing, and
circulation.
• AEMT must understand the pathophysiology of
patient’s problem.

Alexander ch10 lecture

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Alexander ch10 lecture