N434 Final Exam - Perfusion (Shock)
Shock defintion ANS: Syndrome of decreased tissue perfusion and impaired cellular metabolism >
imbalance in supply/demand for oxygen and nutrients > hypoperfusion
When the cells experience hypoperfusion, the demand for oxygen and nutrients exceeds the supply
Cardiogenic shock pathophysiology ANS: there is either systolic or diastolic dysfunction of the heart's
pumping action which results in reduced CO
systolic dysfunction - inability to pump blood forward
diastolic dysfunction - poor filling of the heart
Hypovolemic shock pathophysiology ANS: occurs after loss of intravascular fluid volume
Absolute hypovolemia ANS: fluid lost through hemorrhage, vomiting, diarrhea, fistula drainage,
diabetes insipidus, or diuresis
Relative hypovolemia ANS: Fluids moves out of vascular space into extravascular space (third spacing)
results from bowel obstruction, burns, ascites, fracture of long bone, ruptured spleen, hemothorax,
severe pancreatitis, sepsis
Types of distributive shock ANS: Anaphylactic
Neurogenic
Septic
,Neurogenic shock pathophysiology ANS: SCI results in massive vasodilation without compensation
because of the loss of SNS vasoconstrictor tone > pooling of blood, tissue hypoperfusion, impaired
cellular metabolism
Anaphylactic shock pathophysiology ANS: Life-threatening hypersensitivity reaction > vasodilation,
release of vasoactive mediators, and an increase in capillary permeability > fluid leaks into interstitial
space
Obstructive shock pathophysiology ANS: Physical obstruction to blood flow with decreased CO
Stages of shock ANS: Initial stage
Compensatory stage
Progressive stage
Refractory (irreversible) stage
Initial stage ANS: Usually not clinically apparent
Occurs at cellular level
Metabolism changes from aerobic to anaerobic caused lactic acid build up
Removal of lactic acid ANS: Lactic acid is a waste product removed by the liver
The process requires oxygen
Compensatory stage ANS: SNS activated - attempt to overcome anaerobic metabolism and maintain
hemostasis
, Blood shunted to the brain and heart
Blood shunted away from lungs, kidneys, GI, and skin
Manifestations during compensatory stage ANS: Cardiac - increase in oxygen demands, tachycardia,
hypotension, chest pain
Neuro - confusion
Lungs - increased VQ mismatch, increased RR and depth
GI - risk for paralytic ileus
Kidneys - decreased UOP
Skin - cool, clammy (unless septic shock - they may feel warm)
Progressive stage ANS: Compensatory mechanisms fail
Changes in mental status are important findings during this stage
Aggressive interventions are needed to prevent MODS - move patient to ICU
Cardiac presentation during progressive stage ANS: Continued decreased CO > decrease BP and
coronary artery, cerebral, and peripheral perfusion > altered capillary permeability > leakage of fluid and
protein into interstitial space > diffuse profound edema (anasarca)
Respiratory presentation during progressive stage ANS: Increased pulmonary vascular constriction >
blood low to pulmonary capillaries decreases and ventilation-perfusion mismatch occurs
Tachypnea, crackles, increased WOB
Shock defintion ANS: Syndrome of decreased tissue perfusion and impaired cellular metabolism >
imbalance in supply/demand for oxygen and nutrients > hypoperfusion
When the cells experience hypoperfusion, the demand for oxygen and nutrients exceeds the supply
Cardiogenic shock pathophysiology ANS: there is either systolic or diastolic dysfunction of the heart's
pumping action which results in reduced CO
systolic dysfunction - inability to pump blood forward
diastolic dysfunction - poor filling of the heart
Hypovolemic shock pathophysiology ANS: occurs after loss of intravascular fluid volume
Absolute hypovolemia ANS: fluid lost through hemorrhage, vomiting, diarrhea, fistula drainage,
diabetes insipidus, or diuresis
Relative hypovolemia ANS: Fluids moves out of vascular space into extravascular space (third spacing)
results from bowel obstruction, burns, ascites, fracture of long bone, ruptured spleen, hemothorax,
severe pancreatitis, sepsis
Types of distributive shock ANS: Anaphylactic
Neurogenic
Septic
,Neurogenic shock pathophysiology ANS: SCI results in massive vasodilation without compensation
because of the loss of SNS vasoconstrictor tone > pooling of blood, tissue hypoperfusion, impaired
cellular metabolism
Anaphylactic shock pathophysiology ANS: Life-threatening hypersensitivity reaction > vasodilation,
release of vasoactive mediators, and an increase in capillary permeability > fluid leaks into interstitial
space
Obstructive shock pathophysiology ANS: Physical obstruction to blood flow with decreased CO
Stages of shock ANS: Initial stage
Compensatory stage
Progressive stage
Refractory (irreversible) stage
Initial stage ANS: Usually not clinically apparent
Occurs at cellular level
Metabolism changes from aerobic to anaerobic caused lactic acid build up
Removal of lactic acid ANS: Lactic acid is a waste product removed by the liver
The process requires oxygen
Compensatory stage ANS: SNS activated - attempt to overcome anaerobic metabolism and maintain
hemostasis
, Blood shunted to the brain and heart
Blood shunted away from lungs, kidneys, GI, and skin
Manifestations during compensatory stage ANS: Cardiac - increase in oxygen demands, tachycardia,
hypotension, chest pain
Neuro - confusion
Lungs - increased VQ mismatch, increased RR and depth
GI - risk for paralytic ileus
Kidneys - decreased UOP
Skin - cool, clammy (unless septic shock - they may feel warm)
Progressive stage ANS: Compensatory mechanisms fail
Changes in mental status are important findings during this stage
Aggressive interventions are needed to prevent MODS - move patient to ICU
Cardiac presentation during progressive stage ANS: Continued decreased CO > decrease BP and
coronary artery, cerebral, and peripheral perfusion > altered capillary permeability > leakage of fluid and
protein into interstitial space > diffuse profound edema (anasarca)
Respiratory presentation during progressive stage ANS: Increased pulmonary vascular constriction >
blood low to pulmonary capillaries decreases and ventilation-perfusion mismatch occurs
Tachypnea, crackles, increased WOB
