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

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 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

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

Cardiovascular Response

Surgery1 SGD: SHOCK

C ASE No. 1Salient 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. 2Salient 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