SHOCK - Duke University · Shock Final common pathway of all life whether it be from myocardial...
Transcript of SHOCK - Duke University · Shock Final common pathway of all life whether it be from myocardial...
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SHOCK
May 12, 2011Body and Disease
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Shock
Definition of shock Pathophysiology Types of shock Management of shock
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Shock
Definition?
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Shock
What the Duke Community would have experienced if Gordon Hayward of Butler had hit the last second three point shot in the 2010 NCAA Final
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Shock
What Spike Lee said after Reggie Miller dropped 25 points in the fourth quarter on the Knicks in the 1994 NBA Eastern Conference Finals
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Shock
What you get when you walk across the carpet and pet the cats for a long time and touch the doorknob
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Shock
How Pikachu and other electric Pokemon attack other Pokemon characters
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Shock
“The rude unhinging of the machinery of life” – Samuel Gross 19th Century surgeon
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Shock
Final common pathway of all life whether it be from myocardial infarction, microbial sepsis, pulmonary embolism, trauma, anaphylaxis
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Shock – Pure definition
Inadequate perfusion at the cellular level
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Shock
No substrate for aerobic cellular metabolism
Mitochondria do not have adequate supplies of glucose and oxygen to create ATP
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Shock
Diminished oxygen delivery puts limits on oxygen consumption
Energy output becomes dependent on anaerobic metabolism
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Shock
Decreased ATP Increased lactate production
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Shock
Loss of cellular integrity Normal ion gradients damaged Intracellular fluid increases
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Shock
Loss of Na-K-ATPase pump Acidosis Calcium influx
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Shock
End result – cellular edema and energy deficit lead to cell death and organ dysfunction
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Shock
Vascular endothelial cell damage leads to cytokine and immunomodulator release
Microcirculation damage from continued substrate interruption
Multiple organ system failure
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Shock
Mechanical obstruction of the microcirculation with a loss of lumen diameter and increased osmotic concentration of intravascular material
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Shock
Organs are not able to autoregulate flow Liver failure – deficiency of clotting factors Decreased renal perfusion – increase in
intra and extravascular volume, electrolyte abnormalities
Decrease in lung compliance
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Shock
Cytokine activation Complement activation
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Shock – Treatment Focus
Oxygen delivery Cardiac output Oxygen carrying capacity of the blood
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Treatment
ABCs Vascular access Fluid resuscitation Vasopressors Consider antimicrobials
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Recognition of Shock
High index of suspicion Constant reevaluation
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Recognition of Shock
Level of consciousness Vitals – respiratory rate and effort, heart
rate, pulses Skin perfusion
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Recognition
Level of consciousness
Early – normal or anxious Late – agitated, confused, lethargic
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Recognition
Respiratory rate and effort
Effortless tachypnea
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Recognition
Heart rate
Increased Decreased
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Recognition
Pulses
Weak and thready Early septic shock - bounding
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Recognition
Skin perfusion
Cool, delayed capillary refill time Early septic shock – warm, brisk capillary
refill time
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Hypovolemic Shock
Hemorrhage Dehydration Plasma losses from burns Diabetic ketoacidosis
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Hypovolemic Shock
IV Fluids Blood – type specific cross match
preferred Hypoglycemia
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Distributive Shock
Decreased vascular tone leads to relative vascular volume depletion
Intravascular volume is not distributed properly
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Distributive Shock
Decreased vascular tone results in pooling of blood in the large veins
Decreased venous return results in decreased preload
Cardiac output falls
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Distributive Shock
Anaphylaxis Spinal cord injury
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Distributive Shock
Initial treatment with IV fluids After two to three boluses, consider
vasoactive medications
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Distributive Shock
Dopamine or norepinephrine Alpha adrenergic properties cause
systemic vasoconstriction
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Distributive Shock
Anaphylaxis Epinephrine IM faster and more consistent
uptake Antihistamines Steroids
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Obstructive Shock
Blood is unable to enter or leave the heart even with normal intravascular volume and cardiac function
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Obstructive Shock
Cardiac tamponade Tension pneumothorax Pulmonary hypertension Coarctation of the aorta
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Obstructive Shock
Cardiac tamponade Fluid in the pericardial sac causes
increasing pressure around the heart Increased right atrial pressure causes a
decrease in blood return to the heart Decreased ventricular filling results in
decreased stroke volume
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Obstructive Shock
Most causes of obstructive shock cannot be treated pharmacologically
Look for emergent interventions
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Cardiogenic Shock
Intrinsic dysfunction of the heart and decreased myocardial contractility causes decreased cardiac output
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Cardiogenic Shock
Myocarditis Cardiomyopathies Trauma Dysrhythmias
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Cardiogenic Shock
Treatment is different than other forms of shock
Increased intravascular volume and an increase in systemic vascular resistance increase afterload, increasing the work of the heart
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Cardiogenic Shock
Milrinone Increases inotropy, diastolic relaxation,
and peripheral vasodilation Dobutamine Beta adrenergic with no alpha effects Increases inotropy Decrease in afterload and blood pressure
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Septic Shock
Most controversial Most studied Least understood
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Septic Shock
Multiple organ system derangement Can be considered a form of distributive
shock Also a combination of distributive,
hypovolemic, and cardiogenic shock Host response to the insult is the key
factor
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Septic Shock
Infectious agent Mediators produced by the infectious
agent Response of the immune system to the
infectious agent
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Septic Shock
Responses are usually the result of mediator release
Interleukin-1, tumor necrosis factor-alpha, cytokines, platelet activating factor
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Septic Shock
Warm shock Early septic shock - a hyperdynamic
cardiovascular state with bounding pulses and warm extremities
Despite increased cardiac output, they may be profoundly hypotensive because of decreased systemic vascular resistance
Wide pulse pressure
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Septic Shock
Cold shock Cool, clammy or mottled skin with
diminished or absent pulses and delayed capillary refill time
Cardiac output falls as a result of increased systemic vascular resistance, decreased preload, and myocardial depression
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Septic Shock
ABCs Vascular access Fluid resuscitation Packed red cells Fresh frozen plasma
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Septic Shock
Vasopressor therapy Dopamine Norepinephrine Epinephrine
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Septic Shock
Alpha –smooth muscle contraction in arterioles and bronchiole muscles
Leads to vasoconstriction, increasing blood pressure and afterload
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Septic Shock
Beta -1 receptors mediate contractility (inotropy) and heart rate (chronotropy)
Beta -2 receptors cause smooth muscle relaxation with arteriole vasodilation and bronchiole relaxation
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Septic Shock
Dopamine Combined alpha and beta adrenergic
effects Increase systemic vascular resistance with
vasoconstriction Increase cardiac output with increased
contractility and heart rate
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Septic Shock
Norepinephrine Primarily an alpha agonist Systemic vasoconstriction Anaphylaxis, spinal shock, early septic
shock
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Septic Shock
Epinephrine Potent alpha and beta effects Severe septic shock, post-cardiac arrest
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Septic Shock
Antibiotics Steroids
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Diagnostic Studies
Orders?
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Diagnostic Studies
Blood gas/Shock Panel Bedside glucose Lactate Cultures CBC, chemistries, coags, type and cross CXR, ECG, Echo
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A 25 year old male is brought in by EMS after sustaining multiple gunshot wounds to the chest and abdomen 15 minutes ago.
Vitals BP 70/50, HR 120, RR 35 Listless, responds to verbal stimuli Cool and clammy skin
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A 28 year old construction worker was pinned under debris and was extricated three hours later
Vitals BP nonpalpable, HR 120, RR 10 and shallow
Cyanosis peripherally Unresponsive to verbal stimuli
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Absent breath sounds in the right chest Asymmetric chest wall movement Tracheal deviation to the left Distended neck veins
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An 18 year old male with a history of nut allergies is brought in by EMS for severe respiratory difficulty, and a diffuse red rash.
Vitals BP not obtainable, HR 120, RR 35
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A 5 year old male is brought in by EMS for altered mental status, fever, and a petechial rash on the lower extremities.
Vitals BP 60/palp, HR 140, RR 25 and shallow