SHOCKSHOCK

Case studyCase study You are dispatched to a report of an

overturned bulldozer, trapping a 39 y/o male.

On arrival, you find the patient CAO PPTE. His airway, respirations and pulse are normal. His pelvis and lower extremities are pinned under the side of the bulldozer. The FD tells you it will be at least 10 minutes before they can lift the bulldozer.

HMM??HMM??

The pt. has O2 at 15 lpm/nrb. His BBS are =, clear and he complains that he can’t feel his feet.

Your DDX?

His BP is 110/68, HR 90, RR 24, and Sa02 99%. Because of the extended extrication time, you request Lifeflight response. You establish 2 IV’s w/NS; one at full flow. You check his vitals q 5 min. – they remain stable.

As the bulldozer is lifted, you realize that the pt. has pelvic, bilateral femur and L tibia Fx.

The pt. c/o increased pain, is restless and attempts to get up, then becomes lethargic. His Sa02 is now 94%; his HR is 130 and weak. You increase the IV flow rate, and his mentation improves, but his HR remains elevated.

The pt. is moved to the helicopter, and the IV’s are placed in pressure infuser bags.

At the hospital, his systolic BP is 90, and he is still tachycardic.

The pt. goes to surgery, tolerates the surgery well, and is in rehab for one year.

SHOCKSHOCK

Inadequate Tissue Perfusion

Cells die>tissues die>organs

die>patient dies

The transition between

homeostasis and death

CausesCauses Trauma

spinal cord injury

fluid loss

Infection

Allergic reaction

etc

PerfusionPerfusion

The pump

The fluid

The container

The pumpThe pump Stroke Volume = one beat = 70

mls SV x HR = CO

70 x 80 = 5,600 ml/min Preload Cardiac contractility Afterload

PreloadPreload

Blood delivered to heart during diastole (between contractions) Depends on venous return The greater the preload, the greater

the stroke volume

Contractile forceContractile force

The greater the preload, the more the ventricles are stretched

The greater the stretch (to a point) the greater the contraction Frank - Starling law

Contractile force is affected by catecholamines (controlled by sympathetic nervous system) – affect beta adrenergic receptors

AfterloadAfterload

Arterial resistance (PVR)Vasoconstriction/vasodilation

AfterloadAfterload

Vasopressor drugs

Epinephrine

Dopamine

Norepinephrine

Blood pressureBlood pressure

Baroreceptors Nerve tissue in Carotids & Aorta

Adrenergic responses Low B/P Releases Epi/Norepi Rising B/P slows release of …

Adequate quantity

Adequate quality

BloodBlood

The containerThe container

Closed system –Supposed 2B

Dynamic in nature

Capillaries – Still The Capillaries – Still The ContainerContainer

The Dam Pre-capillary sphincter

Responds to local needs

The Dam Post-capillary sphincter

Peripheral resistancePeripheral resistance

Length of vessel

Diameter of vessel

Viscosity of blood

Oxygen transportOxygen transport

Tidal volume 500-800 mls

21% oxygen in air

Hemoglobin

The Fick PrincipleThe Fick Principle

Adequate concentration inspired

Appropriate diffusion into bloodMore O2 in Stream than cells

The Fick PrincipleThe Fick Principle

Adequate RBCs

Adequate on-loading

The Fick PrincipleThe Fick Principle

Proper perfusion

Adequate off-loading

Brief Relation to Brief Relation to SaOSaO22

Oxygen - Hemoglobin

Saturation

Decreased PerfusionDecreased Perfusion

Pump

Container

Fluid

Decreased perfusion-Decreased perfusion-PumpPump

Inadequate preload

Inadequate contraction

Excessive afterload

Inadequate rate

Inadequate fluidInadequate fluid

Hypovolemia

Inadequate RBCs

Toxic – 3rd Spaced

Inadequate containerInadequate container

Dilated

Constricted

Leaking

Systemic response to Systemic response to shockshock

Early signs

Late signs

Compensated shock – Compensated shock – Initial shock phaseInitial shock phase

Vasoconstriction

Increased cardiac output

Increased contractility

Compensated shock, Compensated shock, cont.cont.

Renin-angiotension system Activated by hypotension Renin released from kidneys into systemic

circulation Acts on special plasma protein angiotension to

produce angiotension I and is converted to angiotension II by enzyme in lungs – angiotension converting enzyme (ACE). – a potent vasoconstrictor.

angiotension II stimulates production of aldosterone from adrenal gland – stimulates kidneys to readsorb sodium (water follows salt)

Compensated shock, Compensated shock, cont.cont.

Pituitary gland secretes ADH Spleen (can store > 300 ml of

blood – can expel up to 200 ml blood into venous circulation

Compensated shock ends with drop in blood pressure

Decompensated shock Decompensated shock (Progressive shock)(Progressive shock)

BP begins to fall Slow refill

Pre-capillary sphincters relax Post-remain closed

No pressure to open Rouleaux

Can’t limbo through capillaries

Bad news, babyBad news, baby

Cardiac depression – 2ndary to compensatory mechanisms – Greatly increased demand for oxygen

Low arterial blood pressure = coronary blood flow too low to adequately perfuse the myocardium

Heart is weakened – CO falls Vasomotor center of brain is depressed

Sympathetic activity slows, then stops

We aint done yetWe aint done yet

Metabolic wastes are released into slower-flowing blood. Capillary beds become aciditic = microemboli Generalized, systemic acidosis

develops Further deterioration of calls and tissues

= increased permeability = shift into 3rd spaces

Irreversible shockIrreversible shock

Death is inevitable

Short term save vs

Long term save

Types of shockTypes of shock

Hypovolemic Distributive Obstructive Cardiogenic Respiratory Neurogenic

AssessmentAssessment

ABCDEs

Intervene early

Hypovolemic ShockHypovolemic Shock Internal or external hemorrhage Traumatic injury Long-bone or open fractures Severe dehydration 2ndary to vomiting or

diarrhea Plasma loss – burns Sweating DKA with osmotic diuresis 3rd spacing –

Bowel obstruction Peritonitis, pancreatitis Liver failure - ascites

Management - Management - HypovolemicHypovolemic

ABCs C-spine O2

ECG IVs PASG?

Distributive shockDistributive shock

Mechanisms prevent appropriate distribution of nutrients and removal of waste products Anaphylactic shock

Histamine causes vasodilation, precapillary sphincter dilation, 3rd spacing, etc.

Septic shock Massive infection

DKA Carbon Monoxide poisoning

Management - Management - DistributiveDistributive

ABCs O2

ECG Iv’s Meds? PASG?

Obstructive shockObstructive shock

Tension pneumothorax Intrathoracic pressure Mediastinal shift

Cardiac tamponade Pulmonary emboli

Management - Management - ObstructiveObstructive

ABCs O2 ECG IV Correct obstruction?

Cardiogenic shockCardiogenic shock

MI Electrical system disturbances Valve failure Cardiac rupture pumping action

May present with s/s AMI, or Pulmonary edema

Management - Management - CardiogenicCardiogenic

If BP is low, what is pulse?

Fluid challenge If lungs are dry

Vasopressors?

Dopamine (Inotropin)

Respiratory shockRespiratory shock

Respiratory system can’t being oxygen into alveoli and remove carbon dioxide Airway obstruction Flail chest Respiratory muscle paralysis Pneumothorax Tension pneumothorax

Management - Management - RespiratoryRespiratory

ABCs O2 ECG IV Correct condition?

Neurogenic shockNeurogenic shock

Interruption in communication pathway between CNS and body Spinal injury Head injury

Artioles dilate, vascular container bigger Fluid driven into interstitial spaces (3d spacing)

Compensatory mechanisms often affected

Skin below injury warm, pink Skin above injury looks shocky

Usually spinal cord injury

Spinal-immobilize

IV fluids

EKG

Management - Management - NeurogenicNeurogenic

Shock AssessmentShock Assessment