[03.13] Surgery_ Shock in Trauma V2.pdf

End result of many different processes

What shock is, not a disease

JBS Haldane

The person who stated, "Shock is the rude unhinging of the delicate machinery of life"

Inadequate to provide perfusion to the vital organs

The condition of systemic blood pressure in shock

Reduction in the mean systemic blood pressure, usually below 70mmHg

One of two requirements for diagnosing shock

Evidence of hypoperfusion of vital organs

One of two requirements for diagnosing shock

Altered mentation and low urine volume

The most important evidences of vital organ hypoperfusion

Increased levels of lactic acid

A finding suggestive of global ischemia resulting in shock

Pallor, thready or non-palpable pulses, mottling

Subtle signs of shock

Hypotension, cool mottled extremities, slow capillary refill

Signs of inadequate oxygen delivery at the organism level in shock

Brain, heart, and lungs

The organs to which the body shunts blood during distress

Cutaneous vasoconstriction

The mechanism by which shunting of blood is done

Altered mental status

Organ-level sign of shock in the brain

Low urine output (oliguria)

Organ-level sign of shock in the kidney

Lactic acidosis

Cellular-level sign of shock, leading to cell injury or death

Pump (Heart), Fluid volume (Blood), Container (Blood vessels or vascular bed)

The three main components of the circulatory system

BP = CO x TPR

Formula for blood pressure

CO = HR x SV

Formula for cardiac output

Volume of blood flow in L/min

What CO stands for in the blood pressure formula

Volume of blood with each ventricular contraction

What SV stands for in the cardiac output formula

Inappropriate vasodilation

What is present in septic shock that results in hypovolemia

Preload, Heart rate, Afterload, Myocardial contractility

Factors affecting cardiac output

Blood in the ventricle at the start of systole that stretches the myocardium

What preload is

High heart rate

What maintains cardiac output during falling blood volume

Resistance against flow out of the ventricle

What afterload is

Decrease in volume

What leads to decreased preload

Central Venous Pressure (CVP)

How preload was previously measured for the right side of the heart

Left Ventricular End-Diastolic Volume (LVEDV)

How preload was previously measured for the left side of the heart

Oxygen

What the brain primarily needs, not blood or glucose

DO2 = CO(L/min) × CaO2(ccO2/dL)

Formula for determination of oxygen delivery

Hemoglobin, Oxygen saturation, Partial pressure of oxygen

The components of arterial oxygen content (CaO2)

MAP = SVR x CO

Formula for organ perfusion pressure

Tied up to our heme

Where the significant amount of oxygen in our blood is predominantly found

Increase cardiac output

What the body can do to compensate for a drastic drop in hemoglobin

Hypovolemic shock

Type of shock due to inadequate blood volume

Cardiogenic shock

Type of shock due to pump failure

Distributive shock

Type of shock that includes neurogenic and anaphylactic shock

Obstructive shock

Type of shock due to physical obstruction to cardiac filling/emptying

Loss of whole blood, loss of plasma, loss of interstitial fluid, severe dehydration

Causes of hypotension in hypovolemic shock

Active bleeding, hemorrhage

Causes of whole blood loss

Extensive burns, dengue

Causes of plasma loss

Diaphoresis, diabetes mellitus, diabetes insipidus, emesis, diuresis

Causes of interstitial fluid loss

Dysentery, gastric outlet obstruction, high output stomas

Causes of severe dehydration leading to hypovolemia

Baroreceptor and chemoreceptor reflexes, circulating vasoconstrictors, reabsorption of interstitial fluid, renal reabsorption of sodium and water, activation of thirst mechanism, shift to the right in O2 dissociation curve

Compensatory mechanisms to maintain perfusion in hypovolemic shock

Carotid sinus and aortic arch

Locations of arterial baroreceptors

CN IX and CN X

The cranial nerves that mediate arterial baroreceptors

Inhibit SNS outflow and stimulate PNS

The normal action of arterial baroreceptors

Activation of SNS and inhibition of PNS

The action of arterial baroreceptors during hemorrhage or low blood volume

Venoatrial junction

The location of baroreceptor reflexes mentioned in relation to ADH

Decreased receptor firing

What happens to baroreceptor firing in hemorrhage that leads to increased ADH release

Water retention and increased vasoconstriction

The effects of increased ADH release during hemorrhage

Decreases blood volume and central venous pressure (CVP)

The initial effect of hemorrhage on CVP

Increased CVP and SV, increased venous return to the heart

The result of peripheral venous constriction decreasing venous compliance

Frank-Starling mechanisms

The mechanism by which increased CVP increases ventricular preload and force of contraction

Increases in CO2 and decreasing O2 levels

What chemoreceptors detect

Sympathetic activation

The result of acidosis stimulating central and peripheral chemoreceptors

Catecholamines from adrenal medulla

What SNS activation triggers the release of, which helps activate RAAS

RAAS

The system that drives fluid retention to reconstitute lost volume

ADH

A potent vasoconstrictor and thirst activator

Angiotensin II, vasopressin, and catecholamines

Hormones that reinforce sympathetic-mediated vasoconstriction

Renin

An enzyme that transforms angiotensinogen into angiotensin I

Shift to the right

The desired shift in the oxygen dissociation curve during shock

More rapid unloading of oxygen from heme molecule

The benefit of a rightward shift in the oxygen dissociation curve

Acidosis (increased H+), fever (increased temp), increased 2-3 DPG

Factors that cause a rightward shift in the oxygen dissociation curve

Low temp, alkalosis, carbon monoxide poisoning, decreased 2-3 DPG

Factors that cause a leftward shift in the oxygen dissociation curve

Skin, skeletal muscle, renal and splanchnic circulations

Circulations where vasoconstriction increases SVR, redistributing blood

Coronary and cerebral circulation

The circulations that are spared during blood redistribution in shock

Hydrostatic Pressure (HP)

The Starling force that pushes fluid out of capillaries

Oncotic pressure (OP)

The Starling force that pulls fluid into capillaries

Net movement into the intravascular space or fluid reabsorption

The net effect on Starling forces in hypovolemia

Filtration

The net effect on the arterial side of capillaries in normal states, where water leaves intravascular space

Reabsorption

The net effect on the venous side of capillaries in normal states, where water moves back into vessels

Lymphatics

What handles fluid not reabsorbed on the venous side

Autoinfusion

The process where blood volume is reconstituted from water taken from the interstitial space

Capillary hydrostatic pressure falls

What causes autoinfusion

Hemodilution and decreased blood viscosity

The result of autoinfusion causing capillary plasma oncotic pressure to fall and hematocrit to fall

Autoregulatory mechanisms

What maintains cerebral perfusion until MAP is below 60 mmHg

Intense sympathetic discharge

What cerebral ischemia produces, several times greater than maximal baroreceptor activation

Compensated, Progressive, Refractory, Decompensated

The four stages of hypovolemia

Class I or II hemorrhage

The classes of hemorrhage typically seen in the compensated stage

Loss of 30-40% of total blood volume

The characteristic blood loss for the progressive stage of hypovolemia

Risk of major dysfunction of organs leading to multiple organ dysfunction

The primary concern in the progressive stage

Uncontrolled blood loss or exsanguinating bleeding

What progressive hypovolemia may be referred to as if compensation fails

Loss of >40% of TBV (>2000mL)

The characteristic blood loss for the refractory stage of hypovolemia

Almost always irreversible and likely fatal

The prognosis for the refractory stage of hypovolemia

Cellular necrosis and multiple organ failure

The outcomes of the refractory stage of hypovolemia

Point of irreversibility

What the refractory stage is described as, due to cellular and vascular muscle death

Myocardial hypoxia, systolic and diastolic dysfunction, arrhythmias

Consequences of impaired coronary perfusion in decompensated shock

Loss of vascular tone causing progressive hypotension and organ hypoperfusion

What sympathetic escape leads to in decompensated shock

Vasoplegia

The condition caused by the abolition of vasoconstriction, flooding capillaries with fluid

Coagulopathy, hypothermia, acidosis

The vicious triad in hemorrhage that contributes to even more shock

Trauma and its management

A time-critical problem, where longer and greater magnitude of blood loss increases death/complication likelihood

Precipitous fall in cardiac function

What occurred after 4 hours of severe hypotension in dog models

Disruption of blood flow, development of cellular hypoxia, depletion of cellular energy stores, promotion of necrotic or apoptotic cell death

Primary pathophysiological effects of hemorrhagic shock

Reperfusion injury, release of inflammatory mediators, mitochondrial damage, cell death, organ and system failures

Secondary pathophysiological effects of hemorrhagic shock

Second peak

The term for early trauma mortality when patients continue to bleed in the OR

Refractory shock/exsanguination, coagulopathy, severe metabolic acidosis

Causes of early trauma mortality

Third peak

The term for late trauma mortality due to nosocomial infections, sepsis, and multiple organ failure

Narrowed pulse pressure, cutaneous vasoconstriction

Subtle signs of shock recognition

Tachycardia, hypotension

Obvious/explicit signs of shock recognition

Level of consciousness (LOC)

An indicator of adequate cerebral blood flow used to assess mentation in hypovolemia