Unit 1 Stress + Shock

Unit Test on Feb 2nd

Receptors that Respond to Acetylcholine

Cholinergic Receptors

Receptors that respond to Norepinepherine

Adrenergic receptors

Sympathetic Nervous System is divided

• Alpha, a1, a2

• Beta, b1, b2

Effects of Alpha 1

Causes Peripheral vasoconstriction

Effects of Alpha 2

causes coronary artery dilation

Effects of Beta 1

Cause increased HR and FOC

Effects of Beta 2

Causes bronchodilation

Somatic Nervous System

controls senses and skeletal muscle

Stress

Non-specific response of the body to any demand made on it physical & emotional

Agonist

Stimulates something

Antagonist

Blocks something

Stressor

Environmental agents responsible for initiating a stress response both endogenous & exogenous stressors

Endogenous

Arise from within the body

Exogenous

Arise outside the body

Eustress

Good stress the body recognizes as pleasurable, like coping mechanisms but can become distress

Distress

Harmful stress like trauma and in some cases be eustress such as sports or kinks

Effects of Fight or Flight Response

1. SNS activated & is an all or non response

2. HR, FOC, & BP increase

3. Bronchodilation occurs increased RR and Depth

4. Skin vasoconstricts, Pt is pale, increased sweat production from glands

5. Pupils dilate = increased visability

6. GI tract vasoconstricts = Nausea

7. Skeletal muscles vasodilate

General Adaption Syndrome (GAS)

• Hans Selye 1920

• Characterizes a three-stage reaction to stressors

• Reactions to both physical & Emotional Stress

3 Stages of Gas

1. Alarm

2. Adaption

3. Exhaustion

Alarm Stage

• CNS stimulation + SNS responds with Fight or Flight

• Results in increased HR, RR, BP, Blood glucose, dilated pupils

• Pituitary gland is stimulated and activates adrenal glands to release catecholamines, cortisol & aldosterone

Adaption (compensation) Stage

• Body begins to adapt to stress + hormone levels being to return to normal

• Catecholamines normalize as adrenal medulla reduces secretions

• Cortex may still release cortisol as part of exhaustion stage

• Is the end of most stress response

Exhaustion Stage

• Stress continues & results in progressive breakdown of comensatory mechanisims + homeostasis which impairs immune response kidney or heart failure

• Marks the onset of other diseases & disease adaptions

Effects of CNS Activating SNS response

• Catecholamines are released as well as

• Dopamine

• norepinepherine

• epinepherine (adrenaline)

Effects of Pituitary gland activating adrenal cortex

Hormones released

• Glucocorticoids (cortisol)

• aldosterone

• Beta endorphins

Effects of Cortisol

• Stimulates gluconeogenesis (creation of glucose)

• Stimulates the breakdown of proteins in muscles, lymphnodes

• Inhibits protein synthesis = immunosuppression

• Inhibits releasse of prostaglandins + Histamine

• Increase in GI secretions = ulcers

Aldersterone

• Pro-inflammatory properties

• Causes reabsorption of H20, Na, and excretion of K

Norepinephrine

• Dopamine is a precursor to NE

• Dopamine is converted to norepinephrine in presynaptic adrenergic neurons and store in synaptic vesicles

Epinephrine

• converted from NE and stored in adrenal medulla

• Once stimulated, adrenal medulla releases 80% epi + 20% NE directly into circulation

Factors that influence adaptability to stress

1. Previous Experience

2. Physiologic Reserve

3. Rapidity of Onset

4. Genes and Age

5. Health Status

6. Nutrition

7. Circadian Rhythm

8. Psychosocial factors

Stress related disorders

• Cardiovascular: CAD (small vessel ischemia), HTN + Stroke

• Musculoskeletal: Tension headaches + Muscle related backaches

• Respiratory: Asthma

• GI: Ulcers, IBS, Ucerative colitis

• Skin: Eczema + Acne

• Endocrine: Diabetes

• CNS: Fatigue, Depression, Insomnia

Shock

• Inadequate tissue perfusion to the cells due to an inability of the circulatory system unable to meet the needs resulting in cellular hypoxia

Effects of Shock

• Lead to a buildup of waste products of metabolisim at the cellular level

• Inadequate perfusion = cellular hypoxia = cellular anoxia = ischemia = necrosis

Categories of Shock

• Hypovolemic

• Cardiogenic

• Obstructive

• Distributive

• Neurogenic

• Vasogenic

Stages of Shock

1. Compensatory Shock

2. Progressive shock

3. Irreversible shock

Compensatory Shock

Body is able to compensate for the decreased perfusion by maintaining enough perfusion to keep organs functioning

Progressive Shock

• Body is no longer able to compensate and blood is moved to vital organs only

• Vicious cycle of tissue deterioration where the shock state causes more shock

Irreversible Shock

• Therapy no use as too much cell death

• Blood is shunted from kidney & liver = organs die

• Heart & brain perfusion are not adequate = complete cell death

• FATAL

Baroreceptors

• Stretch receptors

• 1. Carotid bodies

• 2. Arotic Arch

Ingested Glucose travels

To the Liver

Liver Function for Glucose

• Convert into glycogen

• Store in liver + Muscles

• Blood Sugar decrease = Convert glycogen to glucose

Glycogenolysis

• Glycogen conversion to glucose

• increase blood glucose

Glycogenesis

• Glucose conversion to glycogen

• decrease blood glucose

Gluconeogenesis

• Creation of glucose from a non-glucose/glycogen source

• Increase blood glucose

Decreased blood flow to kidneys = release of

• Renin in bloodstream

• travels to liver

Angiotensin is stored in

The Liver

Angiotensin + Renin

• Angiotensin I

• Travels to the lungs

ACE means

Angiotensin Converting Enzyme

Angiotensin + ACE

• Angiotensin II

• Stimulates receptors on peripheral blood vessels

Effects of Angiotensin II

• Causes vasoconstriction

• Increased blood flow (to kidneys)

Balanced Ventilation Perfusion

• Blood flows in pulmonary capillaries

• Oxygen is being absorbed from alveoli

• Good perfusion

Wasted Perfusion (Imbalanced Ventilation Perfusion)

• Blood flows in pulmonary capillaries

• no Oxygen in alveoli

Causes of Wasted Perfusion

• Asthma

• COPD

• Choking

• Pulmonary Edema

Imbalanced Perfusion

• Wasted Ventilation

• No blood flow in pulmonary capillaries

• Oxygen present alveoli

Pulmonary Shunting

• Increased pressure in pulmonary capillaries

• Pulmonary hypertension occurs

• Pulmonary Edema occurs

Capillary Permeability

• Water gets pushed out by hyrdostatic peressure

• water drawn back in by Osmotic pressure

• Histamine increases permeability

Interstitial Edema

• increased fluid in interstitial zones

• Pulmonary Edema = Fluid in alveoli

Causes of Edema

• No RBC

• No Proteins

• or no WBC

Histamine

• Increases permeability

• Released when exposed to allergens, trauma, etc

Osmoreceptor Locations

• Hypothalamus

• Thirst receptors

Pulse Qualities of Compensatory Shock

• Rapid

• Weak

• Regular

BP Qualities of Compensatory Shock

Normal

Respiratory Qualities of Compensatory Shock

• Rapid

• Shallow

• Regular

Skin Qualities of Compensatory Shock

• Pale

• Cool

• Diaphoretic

Pupil Qualities of Compensatory Shock

• Dilated

• Reactive

LOA/LOC Compensatory Shock

Restless

Kidney Functions Compensatory Shock

Decreased Urine Output

GI Tract Effects Compensatory Shock

• Nausea

• Thirst

Effects of Shock on Capillary Sphincters

• Pre Capillary Sphincter remains open

• Post Capillary Sphincter remains closed

• Blood can enter capillary bed but cant leave

Interstitial Edema

Pulmonary Capillaries leak fluid into alveoli

What prevents Interstitial Edema

The lymphatic system

Pulse Qualities Progressive Shock

• Rapid

• Weak

• Irregular

BP Qualities Progressive Shock

• Low

• narrow pulse pressure

• Pulse Pressure narrows during shock

Respiratory Qualities Progressive Shock

• Decreased Rate

• Decreased Vol

• Regular

• Fine Crackles

Skin Qualities Progressive Shock

• Ashen/Pale

• Cool

• Dry

• Peripheral Cyanosis

Pupil Qualities Progressive Shock

• Equal

• Sluggish

• Dilated

LOC Progressive Shock

DECREASED SIGNIFICANTLY

Kidneys Progressive Shock

• Urine output further decreased

GI Tract Progressive Shock

• Less food

Pulse Qualities Irreversible Shock

• Slow

• irregular

• Absent peripheral pulses

• Arrest

Respiratory Qualities Irreversible Shock

• Slow

• Irregular

• Decreased Vol

• Fine Crackles

Skin Qualities Irreversible Shock

• Cyanotic

• Cold

Blood Pressure Irreversible Shock

FRANK HYPOTENSION

Pupil Qualities Irreversible shock

Dilated Fixed

LOC Irreversible Shock

• unconscious

• coma

Kidneys Irreversible Shock

Complete Shut Down

GI Tract Irreversible Shock

Projectile Vomiting

Shock Treatment GOALS

1. Improve perfusion

2. Improve oxygenation

Shock Treatment

• Mitigate the underlying cause

• Control hemorrhage, anaphyaxis, or cardiogenic problem

• Immediate Transport to hospital & bypass if needed

• give O2 based on SpO2 & ventilate PRN.

• Transport Supine to correct low BP

• if pt is cold one blanket only (cant be too warm)

Why you shouldn’t Warm up a Shock Patient

• Causes peripheral dilation

• blood wont flow to major organs

Local Allergic Rxn

• Cell mediators are released from cells at the site of entry of the antigen

• eg. Cat hair give you a stuffy nose

Systemic Allergic Rxn

• Cell mediators are released from entry site but also at least one other body system

• Eg. Eat dairy & got GI tract issues + wheezing/SOB

Anaphylaxis

• Systemic allergic Rxn which is life threatening

• Hypersensitivity is linked to our immune system & production of IgE immunoglobins

Development of Hypersensitivity

• 1st exposure is when an antigen enters the system and actives the immunoglobin

• IgE bound to mast cells membranes become sensitized mast cells

• 2nd exposure antigen enters the system and attaches to to the IgE on sensitized mast cells

• releases histamine

Types of immunoglobulins

1. IgA - mostly resp/abdo

2. IgG - all over (bacteria +viruses)

3. IgM - mostly blood & lymph

4. IgE - allergic rxn (immune system overreacting)

Degranulization

• The process which mast cells release histamine + cell mediators

Patheophysiology of Anaphylatic attack

1. exposure to allergen tiggers mast cells

2. Histamine release

3. Histamine increases capillary permeabiity

4. Fluid moves into 3rd space (Edema)

5. Histamine dilates blood vessels (decr BP)

6. Leukotrienes also released leading to bronchoconstriction

Manifestations of Acute Allergic Rxn

• Urticaria (hives)

• Tachypnea or SOB

• GI upset

• Reflex tachycardia (with no hypotension)

• Anxiety

Manifestations of life threatening Allergic Rxn

• Angioedema (edema of face, tongue, lips)

• Narrowing upper airway (stridor)

• Bronchoconstriction (wheezing)

• Hypotension

• Reflex Tachycardia (with hypotension)

Physical Assessment Allergic Rxn

• Visualize s+s

• Auscultate

• Vitals (HR, BP, RR)

History Assessment Allergic Rxn

• Were they exposed to a probable allergen?

• History of allergy or anaphylaxsis?

• Medic Alert?

• Do they carry epipen and have they used it?