NRSG 327 FINAL EXAM TEST
COMPLETE 2026 STUDY QUESTIONS
WITH VERIFIED CORRECT SOLUTIONS
GUARANTEED PASS | ASSURED A+
Students also studied
Terms in this set (147)
shock syndrome characterized by decreased tissue perfusion and
impaired cellular metabolism
results in an imbalance btween supply and demand for
oxygen and nutrients
classifications of shock hypovolemic
cardiogenic
distributive (sepsis, anaphylaxis and neurogenic)
Cardiac Output (CO) and calculation Amount of blood pumped in 1 minute (~5 L)
stroke volume x heart rate
preload and what is it determined by? the volume of blood in the ventricles at the end of diastole
determined by:
- venous return
-ability of ventricle to stretch, relax and fill
afterload and what is it determined by? the force, or resistance, against which the ventricles have to
pump in order to eject the blood
3 Vs it is determined by:
-vessel tone
-valve
-viscosity
what is contractility determined by? -preload
-the stimulatory effect of the SNS
-external factors that affect the amount of calcium in
myocardial cell
, What is Starling's Law? Stretching of heart muscle fibers causes increased force of
contraction (e.g., more blood going to heart -> heart
pumps harder> more CO)
In HF - this mechanism doesn't work (more blood coming in,
but heart doesn't pump harder)
Mean arterial pressure equation SBP+2(DBP)/3
Compensated stage of shock -refers to a state in which the body has activated hormonal
and chemical compensatory mechanisms to help maintain
homeostasis
-the body is able to maintain CO and SV
-CELLULAR DAMAGE IS STILL OCCURING
-if it is corrected at this stage, pt will recover
neural compensatory mechanisms in shock SNS activation
-baroreceptors in the aortic arch and carotid bodies sense
changes in blood flow
-stimulates release of epinephrine and norepinephrine
epinephrine mechanism -beta receptors increase HR (chronotropic),
-increases BP (afterload),
-vasoconstriction to legs,
-increase myocardial contractility,
-and bronchodilation.
norepinephrine mechanisms -alpha receptors increase bp (afterload)
-increase vasoconstriction
-secretion of sweat (so does epi)
-inhibits insulin release and stimulates liver to release
glucagon to increase glucose
-stimulates spleen and liver to release RBCs, platelets etc.
biochemical compensatory mechanisms in -chemoreceptors in aortic arch, carotid bodies and medulla
compensatory stage of shock sense decreased pH, O2, and increased CO2
-stimulation causes increase in RR and HR
-CO2 is a powerful vasodilator
hormonal compensatory mechanisms in -RAAS is activated as kidneys sense a decrease in circulating
compensatory stage of shock volume (SNS innervation of kidneys)
COMPLETE 2026 STUDY QUESTIONS
WITH VERIFIED CORRECT SOLUTIONS
GUARANTEED PASS | ASSURED A+
Students also studied
Terms in this set (147)
shock syndrome characterized by decreased tissue perfusion and
impaired cellular metabolism
results in an imbalance btween supply and demand for
oxygen and nutrients
classifications of shock hypovolemic
cardiogenic
distributive (sepsis, anaphylaxis and neurogenic)
Cardiac Output (CO) and calculation Amount of blood pumped in 1 minute (~5 L)
stroke volume x heart rate
preload and what is it determined by? the volume of blood in the ventricles at the end of diastole
determined by:
- venous return
-ability of ventricle to stretch, relax and fill
afterload and what is it determined by? the force, or resistance, against which the ventricles have to
pump in order to eject the blood
3 Vs it is determined by:
-vessel tone
-valve
-viscosity
what is contractility determined by? -preload
-the stimulatory effect of the SNS
-external factors that affect the amount of calcium in
myocardial cell
, What is Starling's Law? Stretching of heart muscle fibers causes increased force of
contraction (e.g., more blood going to heart -> heart
pumps harder> more CO)
In HF - this mechanism doesn't work (more blood coming in,
but heart doesn't pump harder)
Mean arterial pressure equation SBP+2(DBP)/3
Compensated stage of shock -refers to a state in which the body has activated hormonal
and chemical compensatory mechanisms to help maintain
homeostasis
-the body is able to maintain CO and SV
-CELLULAR DAMAGE IS STILL OCCURING
-if it is corrected at this stage, pt will recover
neural compensatory mechanisms in shock SNS activation
-baroreceptors in the aortic arch and carotid bodies sense
changes in blood flow
-stimulates release of epinephrine and norepinephrine
epinephrine mechanism -beta receptors increase HR (chronotropic),
-increases BP (afterload),
-vasoconstriction to legs,
-increase myocardial contractility,
-and bronchodilation.
norepinephrine mechanisms -alpha receptors increase bp (afterload)
-increase vasoconstriction
-secretion of sweat (so does epi)
-inhibits insulin release and stimulates liver to release
glucagon to increase glucose
-stimulates spleen and liver to release RBCs, platelets etc.
biochemical compensatory mechanisms in -chemoreceptors in aortic arch, carotid bodies and medulla
compensatory stage of shock sense decreased pH, O2, and increased CO2
-stimulation causes increase in RR and HR
-CO2 is a powerful vasodilator
hormonal compensatory mechanisms in -RAAS is activated as kidneys sense a decrease in circulating
compensatory stage of shock volume (SNS innervation of kidneys)
