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1. Anestesi - Shock
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Blok : Trauma and Emergency
SHOCKdr. Imam Ghozali., M.Kes, Sp.An
Departemen Ilmu AnestesiFakultas Kedokteran Universitas MalahayatiBandar Lampung
What is Shock?Inadequate perfusion of body tissue that begins at the cellular level and if left untreated results in death of tissue, organs, organ systems, and ultimately the entire organismIT IS NOT LOW BLOOD PRESSURE!
Shock is a result of many reasons:TraumaFluid lossMIInfection
Allergic ReactionSpinal Cord InjuryOther reasons
What is adequate perfusion?Constant and necessary passage of blood through the bodys tissue
Perfusion is dependent on a functioning and intact circulatory system
Components of circulatory system
The pump(heart)The fluid(blood)The container(blood vessels)
The PumpThe Heart is the pump of the cardiovascular systemIt receives blood from the venous system then pumps the blood to the lungs for oxygenation, then to the peripheral tissues
Stroke VolumeThe amount of blood ejected by the heart in one contraction
Factors affecting stroke volumePreloadCardiac Contractile ForceAfterload
PreloadAmount of blood delivered to the heart during diastole
Cardiac Contractile ForceThe strength of contraction of the heartIt is affected by circulating hormones called catecholamines
-Epinepherine-NorEpinepherine
Frank Starling MechanismThe greater the stretch of the cardiac muscle, up to a certain point, the greater the force of cardiac contraction(I.E. the rubber band effect)
AfterloadResistance against which the ventricle must contractDetermined by the degree of peripheral vascular resistance
Cardiac OutputAmount of blood pumped in one contraction
Stroke volume x Heart rate=Cardiac output
Peripheral Vascular ResistancePressure against which the heart must pumpBlood pressure=cardiac output x peripheral vascular resistance
FluidBlood is thicker and more adhesive than waterConsist of plasma and formed elements:
Red cells, White cells, PlateletsTransports oxygen, carbon dioxide, nutrients, hormones, and metabolic wasteAn adequate amount is needed for perfusion
ContainerBlood vessels serve as the containerUnder control of the autonomic nervous system they can adjust size and selectively reroute blood through microcirculationMicrocirculation is comprised of the small vessels:
Arterioles, Capillaries, and Venules
Container contCapillaries have a sphincter between the arteriole and capillary called the pre-capillary sphincterPre-capillary sphincter responds to local tissue demands such as acidosis, hypoxia, and opens as more blood is needed
Post-Capillary SphincterAt the end of the capillary between the capillary and venuleOpens when blood is needed to be emptied into the venous system
Blood Flow RegulationPeripheral Vascular ResistancePressure within the system
Major functions of PerfusionOxygen transportWaste Removal
Inadequate PumpInadequate preloadInadequate cardiac contractile strengthInadequate heart rateExcessive afterload
Inadequate FluidHypovolemia (abnormally low circulating blood volume)
Inadequate ContainerDilated container without change in fluid volumeLeak in container
Shock at cellular levelThe causes of shock vary, however the ultimate outcome is impairment of cellular metabolism
Impaired use of oxygenWhen cells dont receive enough oxygen or cannot use it effectively, they change from aerobic to anaerobic metabolism
Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does not require oxygen). It yields pyruvic acid, with toxic by-products such as lactic acid, and very little energy. (B) Stage two is aerobic (requires oxygen). In a process called the Krebs or citric acid cycle, pyruvic acid is degraded into carbon dioxide and water, which produces a much higher yield of energy.
Compensated and Decompensated shockUsually the body is able to compensate but when these mechanisms fail shock develops and may progress
Compensation MechanismsCatecholamines may be secreted ( I.E. Epinephrine and norepinephrine)The Renin-Angitensin system aids in maintaining blood pressureEndocrine Response by pituitary gland results in secretion of anti-diuretic hormone (ADH)
Catecholamine ReleaseEpinephrine and Norepinephrine release affects the cardiovascular system, causing increase in HR, increase in Cardiac contractility strength, arteriolar constriction which elevates blood pressure
Renin-Angiotensin systemRenin is released from the kidneys and acts on specialized plasma protein called Angiotensin the produces AngiotensinI.AngiotensinI is converted to AngiotensinII by enzymes in the lungs called Angiotensin Converting Enzyme (ACE)
Renin-Angiotensin System (cont)AngiotensinII is a potent vasoconstrictorAngiotensin II stimulates production of aldostrone, which causes the kidneys to reabsorb sodium
Anti-Diuretic HormoneCauses the kidneys to reabsorb water creating an additive to the aldostrone
Compensated ShockEarly stages of shock where the bodys compensatory mechanisms are able to maintain normal perfusion
Decompensated ShockAdvanced stage of shock that occurs when the bodys compensatory mechanisms fail to maintain normal perfusion
Irreversible ShockStage of shock that has progressed to the point that the body nor medical interventions correct the problem
Types of shockCardiogenic shock (Inadequate Pump)Hypovolemic shock (Inadequate Fluid)Neurogenic shock (Inadequate Container)Anaphylactic shock Septic shock
Cardiogenic ShockThe heart loses the ability to supply all body parts with bloodUsually the result of left ventricular failure secondary to acute MI or CHFMany patients will have normal blood pressures
S/S of Cardiogenic ShockMajor difference between other types of shock is presence of Pulmonary EdemaDifficulty breathingWheezes, Crackles, Rales are heard as fluid levels increaseProductive cough with white or pink-tinged foamy sputumCyanosisAltered mentationOliguria ( decreased urination)
TX for Cardiogenic ShockAssure open airwayAdminster oxygen Assist ventilations as neededKeep patient warmPlace patient in position of comfortEstablish Iv with minimal fluid administrationMonitor VitalsMay need to administer Dopamine or Dobutamine
Hypovolemic ShockInternal or external hemorrhageTraumaLong bone or open FXsDehydrationPlasma loss due to burnsExcessive sweatingDiabetic Ketoacidosis with resultant osmotic
diuresis
S/S of Hypovolemic Shock
Pale, cool, clammy skinBlood pressure may be normal then fallPulse may be normal then become rapid, finally slowing and disappearingUrination decreasesCardiac dysrhythmias may occur
Tx for Hypovolemic ShockAirway controlAdminister high flow oxygenControl severe bleeding Keep patient warmElevate lower extremitiesEstablish IV and administer bolus of crystalloid solution for fluid replacement
Neurogenic ShockResults from injury to brain or spinal cord causing interruption of nerve impulses to arteriesArteries lose tone and dilate causing hypovolemiaSympathetic nerve impulses to the adrenal glands are lost, which prevents the release of catecholamines and their compensatory effects
Neurogenic Shock (cont)High cervical injuries cause interruption of impulse to peripheral nervous system causing Neurogenic shock is most commonly due to severe injury to spinal cord or total transection of cord (spinal shock)
S/S of Neurogenic ShockWarm, Dry, Red SkinLow Blood PressureSlow Pulse
TX for Neurogenic ShockAirway controlMaintain body temperatureImmobilization if indicatedConsider other causes of shockIV and medications that increase peripheral vascular resistance (I.E. Norepinephrine, Dopamine)
Anaphylatic ShockSevere immune response to foreign substanceS/S most often occur within minutes but can take up to hours to occurThe faster the reaction develops the more severe it is likely to beDeath will occur if not treated promptly
S/S of Anaphylactic ShockSkin
- Flushing- Itching- Hives-Swelling-Cyanosis
S/S of Anaphylactic ShockRespiratory System
- Breathing difficulty- Sneezing, Coughing- Wheezing, Stridor- Laryngeal edema- Laryngospasm
S/S of Anaphylactic ShockCardiovascular System
- Vasodilation- Increased heart rate- Decreased blood pressure
S/S of Anaphylactic ShockGastrointestinal System
- Nausea, vomiting- Abdominal cramping- Diarrhea
TX for Anaphylactic ShockAirway protection which may include Endotracheal IntubationEstablish IV with crystalloid solutionPharmacological interventions: Epinephrine, Antihistamines(Benadryl), Corticosteroids(dexamethasone), Vasopressors(dopamine, Epinephrine), and inhaled beta agonist(albuterol)
Septic ShockAn infection enters bloodstream and is carried throughout bodyToxins released overcome compensatory mechanismsCan cause dysfunction of one organ system or cause multiple organ dysfunction
S/S of Septic ShockIncreased to low blood pressureHigh fever, no fever, hypothermicSkin flushed, Pale, CyanoticDifficulty breathing and altered lung soundsAltered LOC
TX of Septic ShockAirway controlAdminister oxygenIV of crystalloid solutionDopamine for blood pressure supportMonitor other vitals
Multiple Organ Dysfunction SyndromeMODS is the progressive impairment of two or more systems from and uncontrolled inflammatory response to a severe illness or injury
Progression To MODSInfectionSepsisSeptic shockMODSDeath(if not corrected early)
Primary MODSOrgan damage due to specific cause such as ischemia or inadequate tissue perfusion from shock, trauma, or major surgeryStress and inflammatory responses may be mild or undetectedDuring the response, neutrophils, macrophages, and mast cells are thought to be primed by cytokines
Secondary MODSThe next time there is injury, ischemia, or infection the primed cells are activated, producing and exaggerated inflammatory responseThe inflammatory response enters a self-perpetuating cycle causing damage and vasodilationAnd exaggerated neuroendocrine response is triggered causing futher damage
24 hours post resuscitationLow grade feverTachycardiaDyspneaAltered mental status
Within 24 to 72 hoursPulmonary failure begins
Within 7 to 10 days
Hepatic failure beginsIntestinal failure beginsRenal failure begins
Within 14 to 21 days
Renal and Hepatic failure intensifyGastrointestinal collapseImmune system collapse
After 21 daysHematologic failure beginsMyocardial failure beginsAltered Mental status resulting from Encephalopathy Death