Download N208 Shock and Burns Outline Winter 2013 Systemic Inflammatory

N208 Shock and Burns Outline
Winter 2013
I.
Overview (Visual)
SHOCK (TYPES)
1. Cardiogenic (PUMP gone bad): ↑HR, ↓PP, ↓BP, ↑CVP, ↓CO, ↑PAP
2. Hypovolemic (No GAS in the tank): ↑HR, ↓PP, ↓BP, ↓CVP, ↓CO
a. Absolute (External loss of whole blood)
1. Hemorrhage
2. Surgery
3. GI bleeding
b. Relative (Loss of other body fluids)
1. Vomiting
2. Diarrhea
3. Diabetes Insipidus or melitus
3. Distributive (PIPES gone bad, vascular resistance issues)
a. Neurogenic (spinal cord injury at or above T5, spinal anesthesia, vasomotor
center depression (drugs, hypoglycemia)
↓HR, ↓PP, ↓BP, ↓CVP, ↓PAP, ↓CO
b. Anaphylactic
↑HR, ↓PP, ↓BP, ↓CVP, ↓PAP, ↓CO
c. Septic
↑HR, ↓PP, ↓BP, ↓CVP, ↓ or ↑PAP, ↑ or ↓ CO
4. Obstructive (Indirect Pump Failure): ↑HR, ↓PP, ↓BP, ↑CVP, ↑ or ↓PAP, ↑ or ↓CO
1. Cardiac tamponade
2. Tension Pneumothorax
3. Superior Vena Cava Syndrome
4. Pulmonary Embolism
Systemic Inflammatory Response Syndrome (SIRS)
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Mediator excess: cytokines, oxygen free radicals
Widespread endothelial injury and dysfunction
Vasodilation and increased capillary permeability
Tissue edema
Neutrophil entrapment in microcirculation
Multiple Organ Dysfunction Syndrome (MODS)
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What is shock? Shock is a problem of inadequate supply of oxygen and nutrients to body cells or
inadequate tissue perfusion due to decreased blood flow to body tissues. This is a CELLULAR
phenomenon, not a blood pressure or hemodynamic disturbance.
II.
Compensation versus Decompensation
a. Compensation: Attempts to restore cardiac output to prevent permanent damage to
vital organs after circulatory hemostasis has been altered. Compensatory mechanisms
are activated in an attempt to increase oxygen supply to cells as demand increases: an
individual’s ability to compensate for those demands depends on many factors-age,
comorbidities, extent of initial insult, etc.
1. Sympathetic Nervous System (SNS)
2. Decreased Renal Blood Flow and the SNS activates rennin angiotensin
system-vasoconstriction
3. Glucocorticoids-increased glycogenolysis to increase blood glucose
4. Pulmonary blood flow decreases from the SNS stimulation
ii. Clinical Manifestations (Compensation): What are you going to do about it?
1. Central Nervous System
2. Respiratory
3. Cardiovascular
4. Renal
5. GI
6. Liver
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b. Decompenation-compensatory mechanisms unable to maintain adequate perfusion to
organs (supply unable to meet demands of cells for oxygen and nutrients)
1. Loss of autoregulation in microcirculation-inappropriate
vasoconstriction and vasodilation
2. Ischemic organs
3. Lactic Acid production from anaerobic metabolism
ii. Clinical Manifestations (Decompensation)
1. CNS
2. Respiratory
3. Cardiovascular
4. Renal
5. GI
6. Liver (key organ for clearing bacteria from blood, in making clotting
factors, albumin)
c. Irreversible
i. General hypoxia causing decreased cardiac output (CO) and decreased oxygen
and nutrients to cells
ii. Anaerobic metabolism (Lactic Acid Production)
iii. Clotting abnormalities
iv. Inadequate cerebral blood flow
1. Clinical Manifestations include: CNS (coma), Respiratory arrest (vented),
Cardiovascular (hypotension, poor CO, Tachycardia-bradycardia,
peripheral cyanosis, cold skin), Renal (anuria), DIC
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III.
Diagnostics Studies
a. CBC
1. RBC Count
2. Hematocrit
3. Hemoglobin
b. DIC Screen
c.
d.
e.
f.
g.
h.
i.
j.
k.
l.
IV.
1. Fibrin split products (FSP)
2. Fibrinogen level
3. Platelet count
4. PTT and PT
5. Thrombin time
6. D-Dimer
Creatine Kinase
Troponin
BUN
Creatinine
Glucose
Electrolytes
1. Sodium
2. Potassium
ABG
Blood culture
Lactic Acid
Liver Enzymes (ALT, AST, GGT)
Classification of Shock
a. Hypovolemia Shock (decreased intravascular volume)….Tank is empty!
i. Internal Fluid shifts
ii. External losses of fluid
iii. Pathophysiology: volume depletion, decreased venous return, decreased CO,
decrease blood pressure, cell hypoxia
iv. Clinical Manifestations
1. Decreased cerebral perfusion
2. Decreased systemic perfusion
3. Decreased renal perfusion
4. Decreased peripheral perfusion
v. TREATMENT/Interventions
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b. Cardiogenic Shock-failure of the heart as an effective pump….PUMP FAILURE! (Blood
volume is adequate or increased)
i. Causes:
ii. Pathophysiology:
1. Heart failure-overstretch of myofibrils leads to decreased contractilility
2. Cardiac Tamponade-constrictive effect so ventricle cannot fill during
diastole
iii. Clinical Manifestations
1. Effects of compensation (Tachycardia, vasoconstriction)
2. Effects of decompensation
3. Results
a. Cardiovascular
b. Peripheral Vascular
c. Respiratory
d. Renal
iv. TREATMENT/Interventions:
c. Distributive Shock: Abnormal placement of the vascular volume due to decreased
peripheral resistance and increased intravascular capacity (3 classifications: where
pump and actual blood volume are normal)
i. Neurogenic-massive vasodilation due to loss of sympathetic tone; usually
transitory)
1. Causes:
2. Pathophysiology: Massive vasodilation, both venous and arterial, so BP
drops abruptly
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3. Clinical Presentation (Absence of SNS effects)
a.
b.
c.
d.
Bradycardia and hypotension immediately
Profound change in LOC
Skin warm and dry
Urine output normally initially
4. Treatment/Interventions:
ii. Anaphylactic: massive vasodilation and increased capillary permeability (fluid
leaves vascular space into interstitium, so blood volume actually decreases)
1. Causes: Drugs, iodine dyes (check allergies!), foods, insect bites, blood
products
2. Pathophysiology: antigen/antibody reaction (mediators, such as
histamine, serotonin, prostaglandins, cause vasodilation and leaking
capillaries)
3. Clinical presentation (Circulatory collapse and bronchospasm)
a. Local reactions
b. General reactions
4. Treatment/interventions
iii. Septic
1. Causes:
a. Gram negative bacteria (E. Coli, Klebseilla, serratia,
pseudomonas, proteus, etc….release endotoxin.
b. Gram positive bacteria (staphylococcus, streplococcus,
pneumocacoccus, etc….exotoxin).
c. Viruses
d. Fungi
e. Any microorganism if body’s defenses are impaired
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2. Patients at risk
a. Age (very young and elderly)
b. Malnutrition (alcoholism)
c. Chronic illnesses (diabetes, COPD, chronic renal failure)
d. Immunosuppression (Chemotherapy, steroids, HIV)
e. Invasive catheters (IV, foley, pulmonary artery catheter)
3. Pathophysiology: A host response mediated by hormonal and chemical
substances in reaction to endotoxin, exotoxin or other substances
released by the micro-organism when it dies.
a. Vasodilation
b. Maldistribution of blood volume from selective vasoconstriction
in renal, pulmonary, and skin (heart, brain, skeletal muscle
vasodilate)
c. Myocardial depressant factor, tumor necrosis factor and other
mediators decrease contractility (force of ventricular
contraction)
d. Hormone systems activated
4. Stages of Septic Shock
a. Hyperdynamic (WARM PHASE), patient is warm, flushed, febrile
b. Hypodynamic (COLD PHASE), patient is cold & pale
d. Obstructive Shock: The primary strategy in treating this shock is early recognition and
treatment to relieve or manage the obstruction. Mechanical decompression for
pericardial tamponade, tension pneumo, and hemo pneumo may be done by needle or
tube insertion. Superior vena cava syndrome may be treated with radiation, debulking
or removing the mass or cause. Pulmonary embolism may require thrombolytic therapy
or anticoagulation.
V.
Common Vasoactive Drugs
a. Vasoactive Drugs
i. Receptor type
1. Alpha (action: vasoconstriction)
2. Beta 1 (action: increase heart rate, increased automaticity, conduction
velocity, increased contractility)
3. Beta 2 (action: vasodilation)
4. Dopaminergic (action: Dilation)
b. Vasopressors (constrict peripheral blood vessels)
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c. Vasodilators (dilate arterial or venous beds)
d. Positive Inotropes (increase contractility)
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