SGD - Shock 2
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Transcript of SGD - Shock 2
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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
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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