Summary
Summary Shock, Sepsis, MODS, Burns, and DIC
- Course
- N164 (N164)
- Institution
- Samuel Merritt University
Critical concepts in managing shock, sepsis, multi-organ dysfunction syndrome, burns, and disseminated intravascular coagulation
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N164: Managing Care of Adults IIIShock, Sepsis, MODS, Burns, DIC Ch. 26, 34, 42 W4
SHOCK " Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
" Imbalance in supply/demand for O2 and nutrients
" NO PERFUSION
Categories of Shock
• Cardiogenic shock–Systolic or diastolic dysfunction of the heart’s pumping action results in reduced
cardiac output (CO), stroke volume (SV), and BP. These changes compromise myocardial perfusion,
further depress myocardial function, and decrease CO and perfusion.
• Hypovolemic shock–Inadequate fluid vol. in the intravascular space to support adequate perfusion.
• Distributive shock (Global vasodilation)
o A condition of relative hypovolemia due to intravascular volume redistribution from loss of
vascular tone or disordered permeability.
o Neurogenic shock–Spinal cord injury resulting in massive vasodilation w/o compensation
because of the loss of SNS vasoconstrictor tone. Massive vasodilation leads to a pooling of blood
in the blood vessels, tissue hypoperfusion, and impaired cellular metabolism.
o Anaphylactic shock–Life-threatening hypersensitivity (allergic) reaction to a sensitizing
substance. The reaction quickly causes massive vasodilation, release of vasoactive mediators,
and an increase in capillary permeability. As capillary permeability ↑, fluid leaks from the vascular
space into the interstitial space.
o Septic shock–Profound circulatory, cellular, and metabolic abnormalities. Characterized by
persistent hypotension, despite adequate fluid resuscitation, and inadequate tissue perfusion
that results in tissue hypoxia.
• Obstructive shock–Physical obstruction impeding the filling or outflow of blood resulting in ↓ CO.
Stages of Shock Initial Stage (early stage)
" Occurs at a cellular level
" Usually not clinically apparent–May have warm, flushed skin, resp. alkalosis, ALOC d/t tissue perfusion
• Decreased tissue perfusion
• Lactic acid builds up–Metabolism changes at the cellular level from aerobic to anaerobic, causing
lactic acid buildup. Lactic acid is a waste product that is removed by the liver.
o However, this process requires O2, which is unavailable because of the ↓ in tissue perfusion.
• Metabolic Acidosis
Compensatory Stage (early stage)
" Reversible → Best survival!
• SNS activated (d/t ↓ CO)
o ↑ HR, attempting to compensate for the decreased tissue perfusion
o The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in O2
supply and demand.
• RAAS activated
o Decreased renal blood flow activates RAAS
o Renin stimulates angiotensinogen to make angiotensin I, then converted to angiotensin II.
o Angiotensin II
1. Potent vasoconstrictor ↑ venous return to heart and ↑ in BP
2. Stimulates adrenal cortex to release aldosterone. This results in Na+ and H2O reabsorption
and K+ excretion by the kidneys. ↑ in sodium reabsorption ↑ serum osmolality and
stimulates the release of antidiuretic hormone (ADH). ADH ↑ H2O reabsorption by the
kidneys, further ↑ blood volume. The ↑ in total circulating volume results in ↑ CO and BP.
• Clinical Manifestations
o ↑ RR, ↑HR, ALOC, ↑BGL, ↑Na+, ↓K+
Progressive Stage
" Begins when compensatory mechanisms FAIL
" Transfer to ICU → Changes in mental status are important findings in this stage
" Ischemia
" Lactic acid is profoundly HIGH
" ↑ Capillary permeability
• Cardiovascular system is now profoundly affected
o ↓CO → ↓BP (HYPOTENSION) = A LATE sign of shock!
Refractory Stage → Recovery unlikely
" Profound hypotension and hypoxemia
" Cellular necrosis
" MODS (multiple organ dysfunction syndrome)
" DIC
, Cardiogenic Shock " Systolic or diastolic dysfunction
" Bad pump, but adequate fluid volume
" Compromised cardiac output (CO)
• Causes
o MI
o HF
o Cardiomyopathy
o Cardiac Trauma
• Clinical Manifestations
• Diagnostics " *Symptoms of an MI
o ↑ b-Type natriuretic peptide o Tachycardia
(BNP) & Troponin-T o ↓ BP (Hypotension), SV, CO
o ↑ Blood glucose o ↑ SVR, PAWP, CVP
o ↑ BUN o Narrowed pulse pressure
o ↑ Cardiac biomarkers o ↑ Myocardial O2 consumption (angina)
o Chest x-ray (e.g., pulmonary o Tachypnea, crackles, cyanosis, pulmonary
infiltrates) congestion
o ECG (e.g., dysrhythmias) o Pallor, cool, clammy skin
o Echocardiogram (e.g., left o ↓ Capillary refill time
ventricular dysfunction) o Anxiety, confusion, agitation
o ↓ Renal perfusion, Oliguria (<30mL/hr)
• RN Management
" Overall goal → restore heart function and the balance between O2 supply/demand in the myocardium
o Angioplasty with stenting
o Emergency revascularization
o Valve replacement
o Hemodynamic monitoring
o Drugs to ↓ preload & afterload
o VAD (ventricular assist device) → For advanced stage of HF
Hypovolemic Shock " Inadequate fluid volume (or loss) in the intravascular space to support adequate perfusion
Volume loss may be either absolute or a relative volume loss
1. Absolute Hypovolemia
" Decreased preload due to loss of volume of circulating blood
o External loss of whole blood
• Hemorrhage from trauma, Surgery, GI bleeding, Fistula drainage
o Loss of other body fluids
• Vomiting, diarrhea, Excessive diuresis, Diabetes insipidus (DI), Hyperglycemia
2. Relative Hypovolemia: 3rd Spacing
" Decreased preload due to an increase in the capacity of blood vessels to sequester blood volume
away from the heart, such as with shock from vasodilation.
" Fluid volume moves out of the vascular space into the extravascular space (e.g., intracavitary space)
" We call this type of fluid shift third spacing. One example of relative volume loss is fluid leaking from
the vascular space to the interstitial space from increased capillary permeability, as seen in burns.
o Fluid shifts
• Burn injuries, Ascites
o Internal bleeding
• Fracture of long bones
• Hemothorax
• Organ damage → Ruptured spleen, Severe pancreatitis
° Grey-Turner sign (flank pain)
° Cullen sign (periumbilical ecchymosis)
o Massive vasodilation → Sepsis
o Pooling of blood or fluids → Bowel obstruction
• Clinical Manifestations
" Symptoms of dehydration
o Anxiety
o Tachypnea
o ↑ HR
o ↓ BP (<80 systolic)
o ↓ Urine output (oliguria)
o ↓ CVP, SV, CO, Preload
• RN Management
" Liver produces albumin, patients o IVF (30ml/kg) → Isotonic solutions → LR or NS
with liver failure don’t have o Blood transfusion
albumin which is why the fluid is o Albumin (“volume expander”–a colloid solution that pulls fluid into the blood vessels)
trapped in the peritoneal cavity.
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