Surgery1 SGD: SHOCK

Shock:

failure to meet the metabolic needs of the cell

Initially reversible; irreversible if cellular compensation is no

longer possible

Disruption of the mileu interieur/ homeostasis

Modern Definition:
Inadequate tissue perfusion

decreased delivery of required metabolic substrates

Inadequate removal of cellular waste products

Hypoxemia/ Hypercarbia/ Acidosis

Chemoreceptors: Aorta and carotid bodies

Sensitive to changes in oxygen tension, H+ ion

concentration and carbon dioxide levels

Stimulation
vasodilation of coronary arteries (slower
heart rate)
vasoconstriction of splanchnic and skeletal
circulation
Infection
Change in temperature
Emotional Arounsal
Hypoglycemia
Pain (from injured tissue)

transmitted via spinothalamic tracts

Release of Adrenal Catecholamines via

H-P-Adrenal Axis

ANS: direct sympathetic stimulation

Pathophysiologiy of Shock:

Initial Physiologic Response (imbalance between cellular supply

and demand)

Tissue hypoperfusion

Cellular energy deficit

Neuroendocrine and inflammatory response

Specific responses differ based on etiology

blunted CV response due to sympathetic stimulation in
Neurogenic or Septic Shock
Decreased perfusion can be brought about by cellular
Cardiovascular Response
activation and dysfunction in Septic and Traumatic Shock

Maintain perfusion in Cerebral and Coronary Cirulation;

regulated via
Baro receptors
Chemo receptors
Cerebral ischemic responses
release of endogenous vasoconstrictors
Utilization of extravascular fluid
Renal conservation of salt and water

**See picture of diagrams on iPad Photos

Pathophysiologic Responses vary with time and in response to

resicutation (example in Hemorrhagic Shock)
Compensated Phase

initial loss of blood volume via neuroendocrine

response to maintain hemodynamics
Decompensated Phase

Continued hypo perfusion (may be unrecognized)

cell death and injury; exacerbating factors:

Microcirculatory dysfunction

Parenchymal tissue damage

Inflammatory cell activation

Irreversible Phase

Persistent hypoperfusion further hemodynamic

derangements and cardiovascular collapse

Can develop insidiously

Neuroendocrine and Organ-Specific Response to Hemorrhage

Maintain perfusion to the heart and the brain

Peripheral vasoconstriction
Decrease fluid excretion
Autonomic control

peripheral vascular tone

cardiac contractility
Hormonal reponse to stress and volume deplation
Microcirculatory mechanisms
Afferent Signals

Stimuli from periphery

Loss of circulating blood volume (usually the initial inciting
event)

Baroreceptors: normally inhibit induction of ANS;

inactivated upon stimulation (disinhibition)

Atrial
low volume hemorrhage and mild reductions
in right atrial pressure

Aortic Arch and Carotid bodies

larger reductions in intravascular volume

Surgery1 SGD: SHOCK

C ASE No. 1
Salient Features:

47 year old Male

Admitted to the ER: vehicular accident

Chief Complaint
Blunt injury 30 min PTA
Left side of the chest and abdomen

Conscious, incoherent, disoriented, agitated

Pallor and cold clammy extremities

Vital Signs
Palpatory BP: 70
Faint and thready pulse
RR: 12/ min

Violacious contrusion hematoma over 5th-8th ICS

extends from L mid axillary line to the L midclavicular line

Abdomen: flabby, soft, distended

Agitation whenever palpation is attempted
Structures at the Left Side of the body at the level of 5th 8th ICS

Apex of the heart (Left ventricle)

Lower portion of upper lobe of left lung

Lower lobe of left lung

Spleen

Stomach

Splenic flexure (large intestine)

Left kidney (possibly)

Thoracic Vein Artery Nerve on subcostal (margin? Space?)

Case No. 2
Salient Features:

13 year old boy

Chief Complaint
Continuous RLQ pain

1 week duration
Fever

5 days duration
Vomiting and diarrhea

3 days duration

Lethargic and Disoriented

Vital Signs
BP: 90/70
PR: 110/min
RR: 26/min
T: 39C

(+) rebound tenderness on abdomen over all quadrants