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Complex Final Study Guide latest
2025
Complex Adult Health (Chamberlain University)
NR 341 FINAL EXAM STUDY GUIDE
HEMODYNAMICS:
What is Preload?
The volume of blood stretching the ventricles at the end of diastole (resting phase) before the
next contraction. The filling volume prior to contraction will determine the amount ejected
during systole. Preload can be increased by conditions such as hypertension, aortic valve
disease, and hypervolemia. Preload is decreased when a rapid heart rate or hypovolemia
reduces ventricular filling during diastole.
How do you improve preload?
IV fluids, vasopressors (examples include norepinephrine, epinephrine, vasopressin,
phenylephrine).
What is Afterload?
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The peripheral resistance against which the left ventricle must pump during systole. Afterload
depends on the size of the ventricle, wall tension, and arterial BP. If the arterial BP is elevated,
the ventricles meet increased resistance to ejection of blood, increasing the work demand.
Eventually, this can lead to ventricular hypertrophy, an enlargement of the heart muscle
without an increase in CO or the size of the chambers. Both right and left ventricles work
against resistance, as the right ventricle pumps against afterload of pulmonary artery
resistance.
Systemic vascular resistance (SVR)= afterload for the left ventricle (pushing blood to the body).
Pulmonary vascular resistance (PVR)= afterload for the right ventricle (pushing blood to the
pulmonary artery to the lungs).
How do you improve afterload?
Reduce blood pressure, using vasodilators (examples include nitroglycerine, nitroprusside).
What is Contractility?
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The forcefulness of a myocardial contraction, the force that propels the stroke volume into the
vasculature… the “squeeze” of the muscle.
Contractility can be decreased by hypoxemia (a lack of oxygen, such as with an MI), acidosis,
and beta blockers (decrease the workload of the heart/ relaxes the muscle).
Contractility can be increased by positive inotropes (such as Dopamine and Dobutamine).
How do you improve contractility?
Contractility can be increased by epinephrine and norepinephrine released by the sympathetic
nervous system.
Positive inotropes can also be administered: Dopamine and Dobutamine are examples, these
drugs improve contractility.
What hemodynamic values correlate to preload and afterload?
Central venous pressure, mean arterial pressure, cardiac output, stroke volume, cardiac index.
(Stroke volume (SV)- the amount of blood pumped by the left ventricle per beat.)
What are the normal values for:
*Hemodynamic monitoring is the measurement of pressure, flow, and oxygenation within the
cardiovascular system. The purpose of hemodynamic monitoring is to assess heart function,
fluid balance, and the effects of fluids and drugs on cardiac output.
CVP (central venous pressure) 2-8 mmhg (<2 indicative of hypovolemia, >8 indicative of
hypervolemia). Decreased by dehydration or vasodilation. Increased by fluid overload.
Measured at right atria or superior vena cava, using a central venous line or pulmonary artery
catheter. CVP evaluates right heart function, and right sided preload.
MAP (mean arterial pressure) 70-100 mmhg, in the ICU we will settle for >60-65. Average
arterial pressure during a cardiac cycle. MAP is used to evaluate perfusion to the organs.
Cardiac Output 4-8 liters per minute. The total blood flow through the systemic or pulmonary
circulation per minute. Made up of heart rate and stroke volume.
Cardiac Index ≈2.2/2.5-4.0 liters/ minute/ meter2. More accurate than cardiac output, it is
tailored to individual patient.
What is shock?
Shock is a clinical syndrome which is life-threatening. Shock results in inadequate tissue
perfusion, an oxygen supply less than oxygen demand, and shock affects ALL body systems.
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Shock usually begins with cardiovascular system failure (BP, HR, afterload, etc. Changes).
When shock is present, there will be alterations in at least one of the four components: blood
volume, blood flow, myocardial contraction, vascular resistance.
Identify the stages of shock.
Stage 1- Hypoperfusion Hypoperfusion- inadequate delivery or extraction of
oxygen.
• May have no obvious clinical signs. May see issues with blood
pressure and heart rate, pulmonary issues (low pulse ox.
Reading).
• Early and reversible (antibiotics, fluids, monitoring).
Stage 2- Compensatory Stage 2 will occur if hypoperfusion has went on for a
while… the compensatory mechanisms will begin to
Function.
• Sustained reduction in tissue perfusion.
• Compensatory mechanisms start.
Typical common sign is a significant drop in blood pressure.
Compensatory Mechanisms: The
body will activate neural, hormonal, and biochemical
compensatory mechanisms.
• Baroreceptors and chemoreceptors in the brain, spinal
column, and nervous system.
• Endocrine system, we will look at ACTH and ADH.
• Chemical system: we will see low oxygen, hyperventilation,
respiratory alkalosis.
Seeing any of the symptoms listed above indicates that we are
in stage 2 of shock.
Stage 3- Progressive Compensatory mechanisms fail and the body starts to shut
down.
• Extreme cardiovascular effects: extremity ischemia (usually
starting in lower extremities), cellular hypoxia, lactic acid
production (due to a lack of oxygen and tissue breakdown),
NA+/ K+ failure (these affect muscle contraction).
• Increased capillary hydrostatic pressure.
• Intravascular fluid shifts; interstitial edema and low
circulating volume (low preload).
Downloaded by NELSON KIIRU
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Lom oarc ps d| 26582732
Complex Final Study Guide latest
2025
Complex Adult Health (Chamberlain University)
NR 341 FINAL EXAM STUDY GUIDE
HEMODYNAMICS:
What is Preload?
The volume of blood stretching the ventricles at the end of diastole (resting phase) before the
next contraction. The filling volume prior to contraction will determine the amount ejected
during systole. Preload can be increased by conditions such as hypertension, aortic valve
disease, and hypervolemia. Preload is decreased when a rapid heart rate or hypovolemia
reduces ventricular filling during diastole.
How do you improve preload?
IV fluids, vasopressors (examples include norepinephrine, epinephrine, vasopressin,
phenylephrine).
What is Afterload?
Downloaded by NELSON KIIRU ()
, lOMoAR cPSD| 26582732
The peripheral resistance against which the left ventricle must pump during systole. Afterload
depends on the size of the ventricle, wall tension, and arterial BP. If the arterial BP is elevated,
the ventricles meet increased resistance to ejection of blood, increasing the work demand.
Eventually, this can lead to ventricular hypertrophy, an enlargement of the heart muscle
without an increase in CO or the size of the chambers. Both right and left ventricles work
against resistance, as the right ventricle pumps against afterload of pulmonary artery
resistance.
Systemic vascular resistance (SVR)= afterload for the left ventricle (pushing blood to the body).
Pulmonary vascular resistance (PVR)= afterload for the right ventricle (pushing blood to the
pulmonary artery to the lungs).
How do you improve afterload?
Reduce blood pressure, using vasodilators (examples include nitroglycerine, nitroprusside).
What is Contractility?
Downloaded by NELSON KIIRU
()
, lOMoAR cPSD| 26582732
The forcefulness of a myocardial contraction, the force that propels the stroke volume into the
vasculature… the “squeeze” of the muscle.
Contractility can be decreased by hypoxemia (a lack of oxygen, such as with an MI), acidosis,
and beta blockers (decrease the workload of the heart/ relaxes the muscle).
Contractility can be increased by positive inotropes (such as Dopamine and Dobutamine).
How do you improve contractility?
Contractility can be increased by epinephrine and norepinephrine released by the sympathetic
nervous system.
Positive inotropes can also be administered: Dopamine and Dobutamine are examples, these
drugs improve contractility.
What hemodynamic values correlate to preload and afterload?
Central venous pressure, mean arterial pressure, cardiac output, stroke volume, cardiac index.
(Stroke volume (SV)- the amount of blood pumped by the left ventricle per beat.)
What are the normal values for:
*Hemodynamic monitoring is the measurement of pressure, flow, and oxygenation within the
cardiovascular system. The purpose of hemodynamic monitoring is to assess heart function,
fluid balance, and the effects of fluids and drugs on cardiac output.
CVP (central venous pressure) 2-8 mmhg (<2 indicative of hypovolemia, >8 indicative of
hypervolemia). Decreased by dehydration or vasodilation. Increased by fluid overload.
Measured at right atria or superior vena cava, using a central venous line or pulmonary artery
catheter. CVP evaluates right heart function, and right sided preload.
MAP (mean arterial pressure) 70-100 mmhg, in the ICU we will settle for >60-65. Average
arterial pressure during a cardiac cycle. MAP is used to evaluate perfusion to the organs.
Cardiac Output 4-8 liters per minute. The total blood flow through the systemic or pulmonary
circulation per minute. Made up of heart rate and stroke volume.
Cardiac Index ≈2.2/2.5-4.0 liters/ minute/ meter2. More accurate than cardiac output, it is
tailored to individual patient.
What is shock?
Shock is a clinical syndrome which is life-threatening. Shock results in inadequate tissue
perfusion, an oxygen supply less than oxygen demand, and shock affects ALL body systems.
Downloaded by NELSON KIIRU ()
, lOMoAR cPSD| 26582732
Shock usually begins with cardiovascular system failure (BP, HR, afterload, etc. Changes).
When shock is present, there will be alterations in at least one of the four components: blood
volume, blood flow, myocardial contraction, vascular resistance.
Identify the stages of shock.
Stage 1- Hypoperfusion Hypoperfusion- inadequate delivery or extraction of
oxygen.
• May have no obvious clinical signs. May see issues with blood
pressure and heart rate, pulmonary issues (low pulse ox.
Reading).
• Early and reversible (antibiotics, fluids, monitoring).
Stage 2- Compensatory Stage 2 will occur if hypoperfusion has went on for a
while… the compensatory mechanisms will begin to
Function.
• Sustained reduction in tissue perfusion.
• Compensatory mechanisms start.
Typical common sign is a significant drop in blood pressure.
Compensatory Mechanisms: The
body will activate neural, hormonal, and biochemical
compensatory mechanisms.
• Baroreceptors and chemoreceptors in the brain, spinal
column, and nervous system.
• Endocrine system, we will look at ACTH and ADH.
• Chemical system: we will see low oxygen, hyperventilation,
respiratory alkalosis.
Seeing any of the symptoms listed above indicates that we are
in stage 2 of shock.
Stage 3- Progressive Compensatory mechanisms fail and the body starts to shut
down.
• Extreme cardiovascular effects: extremity ischemia (usually
starting in lower extremities), cellular hypoxia, lactic acid
production (due to a lack of oxygen and tissue breakdown),
NA+/ K+ failure (these affect muscle contraction).
• Increased capillary hydrostatic pressure.
• Intravascular fluid shifts; interstitial edema and low
circulating volume (low preload).
Downloaded by NELSON KIIRU
()
