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REFERENCE shwartz surgery …

REFERENCE shwartz surgery
prepared by dr.kucha

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  • 2. shock• tissue hypoperfusion that is insufficient to maintain normal aerobicmetabolism • consists of inadequate tissue perfusion marked by decreased delivery of required metabolic substrates and inadequate removal of cellular waste products• the resultant cellular injury is initially reversible; if the hypoperfusion issevere enough and prolonged, the cellular injury becomes irriversible• the clinical manifestations are the result of: •stimulation of the sympathetic and neuro-endocrine stress responses • inadequate oxygen delivery • end-organ dysfunction
  • 3. patho-physiology of shock disruption host-microbial trauma equilibrium tissue hypoperfusion neurologic injury cellular hypoxia/ischemia hemorrhage acute heart failure shock
  • 4. neuro-endocrine response to hemorrhage • its goal is to maintain perfusion to the heart and brain , even at the expense of other organ systems • mechanisms include: • autonomic control of peripheral vascular tone and cardiac contractility • hormonal response to stress and volume depletion • local microcirculatory mechanisms that are organ specific and regulate regional blood flowafferent signals• loss of circulating blood volume• pain, hypoxemia, hypercarbia, acidosis,infection, changes in temperature,emotional arousalm, hypoglycemia• baroreceptors • within the atria of the heart which efferent signals are sensitive to changes in chambert- • cardio-vascular response pressure and wall stretch • hormonal response • aortic arch and carotid bodies • circulatory homeostasis• chemoreceptors in the aorta and carotid • microcirculatory responsbodies are sensitive to changes in O2tension, H+ ion concentration, and carbondioxide (CO2) levels • stimulation of the chemoreceptors results in vasodilation of the coronary arteries, slowing of the heart rate, and vasoconstriction of the splanchnic and skeletal circulation• a variety of protein and nonproteinmediators are produced at the site of injuryas part of the inflammatory response, andthey act as afferent impulses to induce ahost response
  • 5. cardio-vascular response• hemorrhage results in diminished venous return to the heart anddecreased cardiac output • stimulation of sympathetic fibers innervating the heart leads to activation of beta1-adrenergic receptors that increase heart rate and contractility • sympathetic stimulation of the peripheral circulation via the activation of alpha1-adrenergic receptors on arterioles induces vasoconstriction and causes a compensatory increase in systemic vascular resistance and blood pressure • sympathetic stimulation also induces constriction of venous vessels, decreasing the capacitance of the circulatory system and accelerating blood return to the central circulation
  • 6. hormonal response• shock hypothalamus (CRH) pituitary gland (ACTH) adrenal cortex (cortisol) • cortisol stimulates gluconeogenesis and insulin resistance, resulting in hyperglycemia • cortisol stimulates muscle cell protein breakdown and lipolysis to provide substrates for hepatic gluconeogenesis • cortisol causes retention of sodium and water by the nephrons of the kidneys• renin-angiotensin system is activated in shock • decreased renal artery perfusion, beta-adrenergic stimulation, and increased renal tubular sodium concentration cause the release of renin from the juxtaglomerular cells • decreased renal •release of renin • renin catalyzes the • angiotensin I has no significant functional artery perfusion from the conversion of activity • beta-adrenergic juxtaglomerular angiotensinogen • angiotensin II stimulation cells (produced by the • a potent vasoconstrictor of both • increased renal liver) to angiotensin splanchnic and peripheral vascular tubular sodium I, which is then beds concentration converted to • stimulates the secretion of cause the release angiotensin II by aldosterone, ACTH, and antidiuretic of renin from the angiotensin- hormone (ADH) juxtaglomerular converting enzyme • aldosterone acts on the cells (ACE) produced in nephron to promote the lung reabsorption of sodium water. • potassium and hydrogen ions are lost in the urine in exchange for sodium.
  • 7. • epinephrine• hypovolemia • angiotensin II • pain• changes in circulating • hyperglycemiablood volume sensed bybaroreceptors and left • pituitary gland releases increase theatrial stretch receptors vasopressin or ADH release of ADH• increased plasmaosmolality detected byhypothalamicosmoreceptors • ADH acts: • on the distal tubule and collecting duct of the nephron to increase water permeability, decrease water and sodium losses, and preserve intravascular volume • as a potent mesenteric vasoconstrictor, shunting circulating blood away from the splanchnic organs during hypovolemia • this may contribute to intestinal ischemia and predispose to intestinal mucosal barrier dysfunction in shock states • increases hepatic gluconeogenesis and increases hepatic glycolysis
  • 8. Microcirculation• the microvascular bed is innervated by the sympathetic nervous system and has a profound effect on the largerarterioles • other vasoactive proteins including: • following hemorrhage • vasopressin larger arterioles • angiotensin II vasoconstrict; small • endothelin-1 distal arterioles vasodilate • also lead to vasoconstriction to limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the GI tract to preserve perfusion of the myocardium and CNS • flow in the capillary bed often is heterogeneous in shock states, which likely is secondary to multiple local mechanisms, including endothelial cell swelling, dysfunction, and activation marked by the recruitment of leukocytes • failure of the integrity of • decreased capillary hydrostatic the endothelium of the pressure secondary to changes in microcirculation and blood flow and increased cellular development of capillary uptake of fluid leak, intracellular swelling, and the development of an extracellular fluid deficit • intracellular swelling is multifactorial, but dysfunction of energy-dependent mechanisms, such as active transport by the sodium-potassium pump contributes to loss of membrane integrity.
  • 9. metabolic effects • cellular metabolism is based primarily on the hydrolysis of adenosine triphosphate (ATP) • majority of ATP is generated in our bodies through aerobic metabolism in the process of oxidative phosphorylation in the mitochondria • dependent on the availability of O2 as a final electron acceptor in the electron transport chain • when oxidative phosphorylation is insufficient, the cells shift to anaerobic metabolism and glycolysis to • O2 tension within a cell decreases, generate ATP there is a decrease in oxidative • this occurs via the breakdown of cellular phosphorylation, and the glycogen stores to pyruvate generation of ATP slows • under hypoxic conditions in anaerobic metabolism, pyruvate is converted into lactate, leading to an intracellular metabolic acidosis • depletion of ATP potentially influences all ATP-dependent cellular processes: • decreased intracellular pH also influences vital cellular functions such as: • maintenance of cellular • normal enzyme activity membrane potential • cell membrane ion exchange • synthesis of enzymes and • cellular metabolic signaling proteins • acidosis leads to changes in calcium metabolism and calcium • cell signaling signaling • DNA repair mechanisms
  • 10. immune and inflammatory responses• a well regulated complex set of interactions betweencirculating soluble factors and cells that can arise inresponse to trauma, infection, ischemia, toxic, orautoimmune stimuli• direct tissue injury or infection• activation of the active inflammatory • intracellular products from damaged and • pattern recognition receptors (PRRs) - cell surfaceand immune responses by the release of injured cells can have paracrine and • Toll-like receptors (TLRs)bioactive peptides by neurons in endocrine-like effects on distant tissues to • receptor for advanced glycation endresponse to pain and the release of activate the inflammatory and immune productsintracellular molecules by broken responses – DANGER SIGNALINGcells, such as heat shock HYPOTHESIS • initiation of the repair process and theproteins, mitochondrial • endogenous molecules (damage mobilization of antimicrobial defenses at thepeptides, heparan sulfate, high mobility associated molecular patterns site of tissue disruptiongroup box 1, and RNA {DAMP}) are capable of signaling • leads to intracellular signaling and release of the presence of danger to cellular products including cytokines surrounding cells and tissues • DAMP: • tissue-based macrophages or mast cells act as • Hyaluronan oligomers sentinel responders, releasing histamines, • Heparan sulfate eicosanoids, tryptases, and cytokines • Extra domain A of fibronectin • Heat shock proteins 60, 70, • Gp96 •Surfactant Protein A - Defensin 2 • Fibrinogen • Biglycan • High mobility group box 1 • Uric acid • Interleukin-1 S-100s Nucleolin
  • 11. Hypovolemic/Hemorrhagic Shock• most common cause of shock in the surgical ortrauma patient is loss of circulating volume fromhemorrhage • acute blood loss • decreased baroreceptor • decreased inhibition of stimulation from stretch vasoconstrictor centers in the brain receptors in the large arteries stem, increased chemoreceptor stimulation of vasomotor centers, and diminished output from atrial • increase vasoconstriction stretch receptors and peripheral arterial resistance • epinephrine and norepinephrine • induces sympathetic stimulation release, activation of the renin- angiotensin cascade, and increased vasopressin release
  • 12. Classification of Hemorrhage ClassParameter I II III IVBlood loss (mL) <750 750–1500 1500–2000 >2000Blood loss (%) <15 15–30 30–40 >40Heart rate (bpm) <100 >100 >120 >140Blood pressure Normal Orthostatic Hypotension Severe hypotensionCNS symptoms Normal anxious confused obtunded, mild tachycardia hypotension, immediately life tachypnea marked threatening, and tachycardia [i.e., generally pulse greater requires than 110 to 120 operative beats per control of minute (bpm)] bleeding
  • 13. • the appropriate priorities in patients with hemorrhagic shock are: • secure the airway • control the source of blood loss • IV volume resuscitation• patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing active hemorrhage from largevessels and require prompt operative intervention • diagnostic and therapeutic laparotomy or thoracotomy• patients who respond to initial resuscitative effort but then deteriorate hemodynamically frequently have injuries that requireoperative intervention• patients who fail to respond to resuscitative efforts despite adequate control of ongoing hemorrhage • have ongoing fluid requirements despite adequate control of hemorrhage • have persistent hypotension despite restoration of intravascular volume necessitating vasopressor support • exhibit a futile cycle of uncorrectable hypothermia, hypoperfusion, acidosis, and coagulopathy that cannot be interrupted despite maximum therapy • these patients have deteriorated to decompensated or irreversible shock with peripheral vasodilation and resistance to vasopressor infusion • mortality is inevitable once the patient manifests shock in its terminal stages• transfusion of packed red blood cells and other blood products is essential in the treatment of patients in hemorrhagic shock • current recommendations in stable ICU patients aim for a target hemoglobin of 7 to 9 g/dL • fresh frozen plasma (FFP) should also be transfused in patients with massive bleeding or bleeding with increases in prothrombin or activated partial thromboplastin times 1.5 times greater than control• additional resuscitative adjuncts in patients with hemorrhagic shock include minimization of heat loss and maintainingnormothermia • development of hypothermia in the bleeding patient is associated with acidosis, hypotension, and coagulopathy • hypothermia in bleeding trauma patients is an independent risk factor for bleeding and death
  • 14. Septic Shock (Vasodilatory Shock)• vasodilatory shock is the result of dysfunction of the endothelium and vasculature secondary to circulatinginflammatory mediators and cells or as a response to prolonged and severe hypoperfusion • hypotension results from failure of the vascular smooth muscle to constrict appropriately• characterized by peripheral vasodilation with resultant hypotension and resistance to treatment withvasopressors• the most frequently encountered form of vasodilatory shock is septic shock • other causes include: • hypoxic lactic acidosis • carbon monoxide poisoning • decompensated and irreversible hemorrhagic shock • terminal cardiogenic shock • postcardiotomy shock • vasodilatory shock seems to represent the final common pathway for profound and prolonged shock of any etiology• in addition to fever, tachycardia, and tachypnea, signs of hypoperfusion such as confusion, malaise, oliguria, orhypotension may be present • these should prompt an aggressive search for infection, including a thorough physical examination, inspection of all wounds, evaluation of intravascular catheters or other foreign bodies, obtaining appropriate cultures, and adjunctive imaging studies, as needed
  • 15. • evaluation of the patient in septic shock begins with an assessment of the adequacy of their airway andventilation • severely obtunded patients and patients whose work of breathing is excessive require intubation and ventilation to prevent respiratory collapse• vasodilation and decrease in total peripheral resistance may produce hypotension • fluid resuscitation and restoration of circulatory volume with balanced salt solutions is essential• empiric antibiotics must be chosen carefully based on the most likely pathogens (gram-negative rods, gram-positive cocci, and anaerobes) because the portal of entry of the offending organism and its identity may not beevident until culture data return or imaging studies are completed • knowledge of the bacteriologic profile of infections in an individual unit can be obtained from most hospital infection control departments and will suggest potential responsible organisms • antibiotics should be tailored to cover the responsible organisms once culture data are available, and if appropriate, the spectrum of coverage narrowed• after first-line therapy of the septic patient with antibiotics, IV fluids, and intubation if necessary, vasopressorsmay be necessary to treat patients with septic shock • catecholamines are the vasopressors used most often• hyperglycemia and insulin resistance are typical in critically ill and septic patients, including patients withoutunderlying diabetes mellitus