Northwest Community Healthcare EMT Training Program - Shock

Vocabulary practice flashcards covering terminology, formulas, physiological responses, shock categories, types, stages, and age-specific baseline values from the Northwest Community Healthcare EMT Training Program notes on Shock.

Shock (Hypoperfusion)

Inadequate tissue perfusion.

Cardiac Output Formula

$$\text{CO} = \text{HR} \times \text{SV}$$

Preload

The amount of blood available for ventricular filling; a decrease in preload reduces stroke volume and cardiac output.

Anaerobic Metabolism

Cellular energy production occurring without adequate oxygen and glucose, leading to acid buildup, failure of the cellular sodium-potassium pump, fluid entering cells, and cellular death.

Alpha1 Receptor Stimulation

Causes vasoconstriction, sweat gland stimulation, and iris muscle contraction, presenting clinically as pale, cool, moist (clammy) skin and pupil dilation.

Alpha2 Receptor Stimulation

Causes decreased insulin production, glucagon release, and conversion of noncarbohydrate sources into sugar.

Beta1 Receptor Stimulation

Causes increased heart rate and increased contractility (force of cardiac contraction), recognized clinically as tachycardia and a bounding pulse.

Beta2 Receptor Stimulation

Causes dilation of the bronchioles, which helps remove $\text{CO}_2$ from cells and move $\text{O}_2$ to cells.

Norepinephrine

A hormone whose Alpha1 effects cause vasoconstriction and sweat gland stimulation, presenting as pale, cool, moist (clammy) skin.

Antidiuretic Hormone (Vasopressin)

A hormone that increases sodium reabsorption in the kidneys to reabsorb water and restore fluid, resulting in decreased urine output and waste buildup that increases blood acidity.

Angiotensin II

A hormone that produces vasoconstriction, increased heart rate, and sodium reabsorption in the kidneys.

Aldosterone

A hormone causing sodium reabsorption in the kidneys, resulting in decreased urine output.

Glucagon

A hormone that converts liver glycogen and noncarbohydrates to blood glucose and increases heart rate and cardiac contractility.

Hypovolemic Shock

Shock caused by low blood volume due to blood loss or fluid loss.

Distributive Shock

Shock caused by a decrease in intravascular volume due to massive systemic vasodilation and increased capillary permeability, reducing systemic vascular resistance and preload without actual initial blood loss.

Cardiogenic Shock

Shock caused by ineffective pump function of the heart, resulting in decreased stroke volume, cardiac output, systolic blood pressure, and tissue perfusion.

Obstructive Shock

Shock caused by a mechanical obstruction or compression impeding forward blood flow despite adequate volume, normal vessel tone, and undamaged heart muscle.

Metabolic or Respiratory Shock

Shock caused by an inability of oxygen to diffuse into blood, be carried by hemoglobin, offload at the cells, or be used effectively in cellular metabolism.

Hemorrhagic Hypovolemic Shock

Shock resulting from whole blood loss from the intravascular space, reducing preload, cardiac output, systolic blood pressure, and red blood cells needed for oxygen delivery.

Nonhemorrhagic Hypovolemic Shock

Shock resulting from intravascular fluid loss (water, plasma proteins, electrolytes) while red blood cells and hemoglobin remain in the vessels.

Burn Shock

A specific form of nonhemorrhagic hypovolemic shock where burn injuries damage capillary integrity, causing plasma and plasma proteins to leak into the interstitial space.

Anaphylactic Shock

A form of distributive shock caused by chemical mediators (such as histamine) that cause massive systemic vasodilation, fluid leakage into interstitial spaces, and severe bronchoconstriction.

Epinephrine (Anaphylaxis Concentration)

Administered at a concentration of $1\,\text{mg} / 1\,\text{ml}$ for anaphylactic shock to induce systemic vasoconstriction (Alpha1) and bronchiole relaxation (Beta2).

Septic Shock

A form of distributive shock caused by an infection releasing bacteria or toxins into the blood, leading to massive vasodilation, permeable capillaries, fluid loss, and often fever.

Neurogenic Shock (Vasogenic Shock)

A form of distributive shock caused by a spinal cord injury damaging sympathetic nerve fibers, causing widespread vasodilation and flushed warm dry skin below the level of injury.

Compensated Shock

An early stage of shock during which the body's compensatory mechanisms maintain a near-normal blood pressure and vital organ perfusion.

Decompensated Shock (Progressive Shock)

An advanced stage of shock where compensatory mechanisms fail to maintain blood pressure and vital organ perfusion, leading to acidosis, organ failure, and hypoxic brain dysfunction.

Irreversible Shock

The terminal stage of shock where organ damage and failure are so extensive that death cannot be prevented or reversed despite aggressive medical intervention.

Lowest Acceptable Systolic BP (Less than 1 year)

$$60\,\text{mmHg}$$

Lowest Acceptable Systolic BP (1 to 10 years)

$$\text{Age in years} \times 2 + 70\,\text{mmHg}$$

Lowest Acceptable Systolic BP (Greater than 10 years)

$$90\,\text{mmHg}$$