SHOCK

Case 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?? 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.

SHOCK Inadequate Tissue Perfusion Cells die>tissues die>organs die>patient dies The transition between homeostasis and death

Causes Trauma spinal cord injury fluid loss Infection Allergic reaction etc

Perfusion The pump The fluid The container

The pump Stroke Volume = one beat = 70 mls SV x HR = CO 70 x 80 = 5,600 ml/min Preload Cardiac contractility Afterload

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

Contractile 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

Arterial resistance (PVR) Afterload Arterial resistance (PVR) Vasoconstriction/vasodilation

Afterload Vasopressor drugs Epinephrine Dopamine Norepinephrine

Blood pressure BP Baroreceptors Adrenergic responses Nerve tissue in Carotids & Aorta Adrenergic responses Low B/P Releases Epi/Norepi Rising B/P slows release of …

Blood Adequate quantity Adequate quality

The container Closed system –Supposed 2B Dynamic in nature

Capillaries – Still The Container The Dam Pre-capillary sphincter Responds to local needs The Dam Post-capillary sphincter

Peripheral resistance Length of vessel Diameter of vessel Viscosity of blood

Oxygen transport Tidal volume 500-800 mls 21% oxygen in air Hemoglobin

Adequate concentration inspired Appropriate diffusion into blood The Fick Principle Adequate concentration inspired Appropriate diffusion into blood More O2 in Stream than cells

The Fick Principle Adequate RBCs Adequate on-loading

The Fick Principle Proper perfusion Adequate off-loading

Brief Relation to SaO2 Oxygen - Hemoglobin Saturation

Decreased Perfusion Pump Container Fluid

Decreased perfusion-Pump Inadequate preload Inadequate contraction Excessive afterload Inadequate rate

Inadequate fluid Hypovolemia Inadequate RBCs Toxic – 3rd Spaced

Inadequate container Dilated Constricted Leaking

Systemic response to shock Early signs Late signs

Compensated shock Vasoconstriction Increased cardiac output Increased contractility

Compensated shock, 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, cont. Pituitary gland secretes ADH Spleen (can store > 300 ml of blood – can expel up to 200 ml blood into venous circulation

Decompensated 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, 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 ain’t 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 shock Death is inevitable Short term save vs Long term save

Types of shock Hypovolemic Distributive Obstructive Cardiogenic Respiratory Neurogenic

Assessment ABCDEs Intervene early

Hypovolemic 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 - Hypovolemic ABCs C-spine O2 ECG IVs PASG?

Management - Distributive ABCs O2 ECG Ivs Meds? PASG?

Management - Obstructive ABCs O2 ECG IV Correct obstruction?

Management - Cardiogenic If BP is low, what is pulse? Fluid challenge If lungs are dry Vasopressors? Dopamine (Inotropin)

Management - Respiratory ABCs O2 ECG IV Correct condition?

Management - Neurogenic Usually spinal cord injury Spinal-immobilize IV fluids EKG

Shock Assessment