NRSG 327 FINAL EXAM WITH VARIFIED
QUESTIONS AND ANSWERS
shock - CORRECT ANSWERS-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 - CORRECT ANSWERS-hypovolemic
cardiogenic
distributive (sepsis, anaphylaxis and neurogenic)
Cardiac Output (CO) and calculation - CORRECT ANSWERS-Amount of blood pumped in 1 minute (~5 L)
stroke volume x heart rate
preload and what is it determined by? - CORRECT ANSWERS-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? - CORRECT ANSWERS-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? - CORRECT ANSWERS--preload
-the stimulatory effect of the SNS
-external factors that affect the amount of calcium in myocardial cell
What is Starling's Law? - CORRECT ANSWERS-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 - CORRECT ANSWERS-SBP+2(DBP)/3
Compensated stage of shock - CORRECT ANSWERS--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 - CORRECT ANSWERS-SNS activation
-baroreceptors in the aortic arch and carotid bodies sense changes in blood flow
-stimulates release of epinephrine and norepinephrine
epinephrine mechanism - CORRECT ANSWERS--beta receptors increase HR (chronotropic),
-increases BP (afterload),
,-vasoconstriction to legs,
-increase myocardial contractility,
-and bronchodilation.
norepinephrine mechanisms - CORRECT ANSWERS--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 compensatory stage of shock - CORRECT ANSWERS--
chemoreceptors in aortic arch, carotid bodies and medulla sense decreased pH, O2, and increased CO2
-stimulation causes increase in RR and HR
-CO2 is a powerful vasodilator
hormonal compensatory mechanisms in compensatory stage of shock - CORRECT ANSWERS--RAAS is
activated as kidneys sense a decrease in circulating volume (SNS innervation of kidneys)
RAAS system - CORRECT ANSWERS--kidneys release renin
-renin converts angiotensinogen to angiotensin I
-ACE converts I to angiotensin II, which is a powerful vasoconstrictor. (it increases afterload and bp)
-AII stimulates pituitary to release ADH (vasopressin) causing vasoconstriction
(increasing afterload and BP)
-AII also stimulates adrenal cortex to stimulate release of aldosterone (increasing blood volume and
preload)
, signs and symptoms in the compensatory stage of shock - CORRECT ANSWERS--skin normal or slightly
pale, cool periphery
-increased RR (chemoreceptors), normal WOB, normal SPO2
-thirst
-slightly restless, possible mild confusion, decreased concentration, increased glucose
-mild tachycardia, strong pulses centrally, possible slightly weaker peripherally, normal bp (decreased bp
is one of the first changes)
-decrease urine output, urine conc, hypoactive bowels
uncompensated (progressive ) stage of shock - CORRECT ANSWERS--stage when compensatory
mechanisms fail
-O2 supply and demand becomes imbalanced
-decreased cellular perfusion =decreased O2/glucose delivery
and leads to inability to remove waste
-accumulation of CO2= vasodilation
what happens when there is decreased perfusion? - CORRECT ANSWERS--less o2 delivery
-cell functions fail the Na/K pump so more Na in cell therefore more water therefore more swelling
-cells in cardiovascular system fail; fluid leaks into interstitial spaces and lungs leading to anasarca
-body switches from aerobic to anaerobic metabolism because of lack of o2. this leads to buildup of
lactic acid leading to acidosis
-acidosis interferes with hgb, and makes arterioles less responsive to epi/norepi
-acidosis also reduces contractility and interferes with clotting
-CO2 will also start to accumulate, causing vasodilation, venous pooling and formation of blood clots in
our microcirculation
QUESTIONS AND ANSWERS
shock - CORRECT ANSWERS-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 - CORRECT ANSWERS-hypovolemic
cardiogenic
distributive (sepsis, anaphylaxis and neurogenic)
Cardiac Output (CO) and calculation - CORRECT ANSWERS-Amount of blood pumped in 1 minute (~5 L)
stroke volume x heart rate
preload and what is it determined by? - CORRECT ANSWERS-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? - CORRECT ANSWERS-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? - CORRECT ANSWERS--preload
-the stimulatory effect of the SNS
-external factors that affect the amount of calcium in myocardial cell
What is Starling's Law? - CORRECT ANSWERS-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 - CORRECT ANSWERS-SBP+2(DBP)/3
Compensated stage of shock - CORRECT ANSWERS--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 - CORRECT ANSWERS-SNS activation
-baroreceptors in the aortic arch and carotid bodies sense changes in blood flow
-stimulates release of epinephrine and norepinephrine
epinephrine mechanism - CORRECT ANSWERS--beta receptors increase HR (chronotropic),
-increases BP (afterload),
,-vasoconstriction to legs,
-increase myocardial contractility,
-and bronchodilation.
norepinephrine mechanisms - CORRECT ANSWERS--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 compensatory stage of shock - CORRECT ANSWERS--
chemoreceptors in aortic arch, carotid bodies and medulla sense decreased pH, O2, and increased CO2
-stimulation causes increase in RR and HR
-CO2 is a powerful vasodilator
hormonal compensatory mechanisms in compensatory stage of shock - CORRECT ANSWERS--RAAS is
activated as kidneys sense a decrease in circulating volume (SNS innervation of kidneys)
RAAS system - CORRECT ANSWERS--kidneys release renin
-renin converts angiotensinogen to angiotensin I
-ACE converts I to angiotensin II, which is a powerful vasoconstrictor. (it increases afterload and bp)
-AII stimulates pituitary to release ADH (vasopressin) causing vasoconstriction
(increasing afterload and BP)
-AII also stimulates adrenal cortex to stimulate release of aldosterone (increasing blood volume and
preload)
, signs and symptoms in the compensatory stage of shock - CORRECT ANSWERS--skin normal or slightly
pale, cool periphery
-increased RR (chemoreceptors), normal WOB, normal SPO2
-thirst
-slightly restless, possible mild confusion, decreased concentration, increased glucose
-mild tachycardia, strong pulses centrally, possible slightly weaker peripherally, normal bp (decreased bp
is one of the first changes)
-decrease urine output, urine conc, hypoactive bowels
uncompensated (progressive ) stage of shock - CORRECT ANSWERS--stage when compensatory
mechanisms fail
-O2 supply and demand becomes imbalanced
-decreased cellular perfusion =decreased O2/glucose delivery
and leads to inability to remove waste
-accumulation of CO2= vasodilation
what happens when there is decreased perfusion? - CORRECT ANSWERS--less o2 delivery
-cell functions fail the Na/K pump so more Na in cell therefore more water therefore more swelling
-cells in cardiovascular system fail; fluid leaks into interstitial spaces and lungs leading to anasarca
-body switches from aerobic to anaerobic metabolism because of lack of o2. this leads to buildup of
lactic acid leading to acidosis
-acidosis interferes with hgb, and makes arterioles less responsive to epi/norepi
-acidosis also reduces contractility and interferes with clotting
-CO2 will also start to accumulate, causing vasodilation, venous pooling and formation of blood clots in
our microcirculation
