NR 341 Critical Care Exam 2 Review
Chapter 8: Hemodynamics
● Central Venous Pressure (CVP)
○ How assessed
■ Need central line that goes into right atrium
■ Arterial lines are placed in the radial (most common), brachial, or femoral artery.
■ The integrity of the arterial waveform should be assessed to verify the accuracy of blood pressure readings.
■ Monitor circulation in the limb with the arterial line (capillary refill, temperature, color).
■ Assesses preload of the right side of the heart.
○ Normal levels
■ CVP/ Right atrial pressure (RAP)
● 2-6
■ Cardiac output (CO)
● HR x SV
● 4-8
■ Stroke Volume
● 60 - 130
■ SVR
● 770 - 1500
○ Causes of abnormal levels
■ Low CVP = dehydration, hypovolemia, vasodilation from medications, rewarming, or sepsis.
■ High CVP = hypervolemia, severe vasoconstriction, mechanical ventilation, pulmonary hypertension, HF.
○ Treatment
● to prevent venous air embolisms->place patient in trendelenburg to increase CVP and ask them to
bear down, (valsalva manuver) while the catheter system is open to air
● pulmonary hypertension -> oxygen first
● hypervolemia ->with chlorothiazide (diuril) or Amiloride ( Midamor)
● decrease in right ventricular compliance from ischemia, hypertrophy,cardiomyopathy, tamponade
or severe acidosis, use->epinephrine or vasopressin
, ○
Chapter 12: Shock, Sepsis and Multiple Organ Dysfunction Syndrome
● Stages of Shock:
○ Expected findings during the compensatory stage (Stage II)
■ During this stage, symptoms become apparent, but shock may still be reversed with minimal morbidity if
appropriate interventions are initiated.
■ Baroreceptors = increased HR (systemic vasoconstriction)
■ Chemoreceptors = breathing harder and deeper (respiratory alkalosis)
■ ACTH = cortisol
■ Skin: pressure ulcers, skin breakdown
■ GI: constipation, peptic ulcers
■ Liver: enzymes elevated
○ Stages of Shock – What happens in each stage
■ Initiation: process of shock is initiated by hypoperfusion, no obvious clinical indication
■ Compensatory: reduction in tissue perfusion initiates a set of neural, endocrine, and chemical
compensatory mechanisms to try in maintain blood flow to vital organs
■ S/S: +HR, narrowed pulse, respiratory alkalosis, thirst, cool moist skin, oliguria, diminished bowel sounds,
restlessness progressing to confusion, hyperglycemia, +urine specific gravity and - creatinine
● Neural: baroreceptors and chemoreceptors detect reduction in arterial pressure and relay message
to medulla oblongata which stimulates the release of epinephrine and norepinephrine.
○ +HR, + contractility, dilation of coronary arteries to + perfusion, systemic
vasoconstriction and redistribution of blood, arterial vasoconstriction= +BP, venous
vasoconstriction= + venous return to heart> + preload> + cardiac output;
Bronchodilation= +RR and depth, + glucose (liver converts glycogen to glucose for
energy), dilation of pupils, peripheral vasoconstriction= cool, moist skin
● Endocrine
○ Reduction in BP> hypothalamus stimulates anterior and posterior pituitary gland; anterior
releases ACTH (glucocorticoid and mineralocorticoids) which + glucose and BP through
releases of renin and angiotensin system. Posterior releases ADH which + intravascular
blood volume and glucose for energy.
● Chemical
○ Low oxygen tension, hyperventilation and respiratory alkalosis
○ Chemoreceptors are stimulated in response to low oxygen in the blood, rate and depth of
respiration +, px hyperventilates> respiratory alkalosis> vasoconstriction of cerebral
blood vessel= can lead to cerebral hypoxia and ischemia
■ Progressive: if hypoperfusion is not corrected px deterioration begins
● Progressive tissue hypoperfusion, anaerobic metabolism with lactic acidosis> metabolic acidosis,
anaerobic produces less ATP which results in failure of Na/K pump, this leads to cellular edema.
● s/s: dysrhythmia, -BP w/ narrowed pulse, tachypnea, cold, clammy skin, anuria, absent bowel
sounds, lethargy, hyperglycemia, +BUN/creatinine/K, respiratory/metabolic acidosis
■ Refractory: Prolonged inadequate tissue perfusion
● Unresponsive to therapy
● Contributes to multiple organ dysfunction and death
○ Hypovolemic Shock:
■ Causes
● Hemorrhage or severe dehydration, burns
■ Signs and Symptoms
● Increased HR, decreased BP, decreased CVP, skin is cool
● Tachypnea, oliguria, decreased mental status
Chapter 8: Hemodynamics
● Central Venous Pressure (CVP)
○ How assessed
■ Need central line that goes into right atrium
■ Arterial lines are placed in the radial (most common), brachial, or femoral artery.
■ The integrity of the arterial waveform should be assessed to verify the accuracy of blood pressure readings.
■ Monitor circulation in the limb with the arterial line (capillary refill, temperature, color).
■ Assesses preload of the right side of the heart.
○ Normal levels
■ CVP/ Right atrial pressure (RAP)
● 2-6
■ Cardiac output (CO)
● HR x SV
● 4-8
■ Stroke Volume
● 60 - 130
■ SVR
● 770 - 1500
○ Causes of abnormal levels
■ Low CVP = dehydration, hypovolemia, vasodilation from medications, rewarming, or sepsis.
■ High CVP = hypervolemia, severe vasoconstriction, mechanical ventilation, pulmonary hypertension, HF.
○ Treatment
● to prevent venous air embolisms->place patient in trendelenburg to increase CVP and ask them to
bear down, (valsalva manuver) while the catheter system is open to air
● pulmonary hypertension -> oxygen first
● hypervolemia ->with chlorothiazide (diuril) or Amiloride ( Midamor)
● decrease in right ventricular compliance from ischemia, hypertrophy,cardiomyopathy, tamponade
or severe acidosis, use->epinephrine or vasopressin
, ○
Chapter 12: Shock, Sepsis and Multiple Organ Dysfunction Syndrome
● Stages of Shock:
○ Expected findings during the compensatory stage (Stage II)
■ During this stage, symptoms become apparent, but shock may still be reversed with minimal morbidity if
appropriate interventions are initiated.
■ Baroreceptors = increased HR (systemic vasoconstriction)
■ Chemoreceptors = breathing harder and deeper (respiratory alkalosis)
■ ACTH = cortisol
■ Skin: pressure ulcers, skin breakdown
■ GI: constipation, peptic ulcers
■ Liver: enzymes elevated
○ Stages of Shock – What happens in each stage
■ Initiation: process of shock is initiated by hypoperfusion, no obvious clinical indication
■ Compensatory: reduction in tissue perfusion initiates a set of neural, endocrine, and chemical
compensatory mechanisms to try in maintain blood flow to vital organs
■ S/S: +HR, narrowed pulse, respiratory alkalosis, thirst, cool moist skin, oliguria, diminished bowel sounds,
restlessness progressing to confusion, hyperglycemia, +urine specific gravity and - creatinine
● Neural: baroreceptors and chemoreceptors detect reduction in arterial pressure and relay message
to medulla oblongata which stimulates the release of epinephrine and norepinephrine.
○ +HR, + contractility, dilation of coronary arteries to + perfusion, systemic
vasoconstriction and redistribution of blood, arterial vasoconstriction= +BP, venous
vasoconstriction= + venous return to heart> + preload> + cardiac output;
Bronchodilation= +RR and depth, + glucose (liver converts glycogen to glucose for
energy), dilation of pupils, peripheral vasoconstriction= cool, moist skin
● Endocrine
○ Reduction in BP> hypothalamus stimulates anterior and posterior pituitary gland; anterior
releases ACTH (glucocorticoid and mineralocorticoids) which + glucose and BP through
releases of renin and angiotensin system. Posterior releases ADH which + intravascular
blood volume and glucose for energy.
● Chemical
○ Low oxygen tension, hyperventilation and respiratory alkalosis
○ Chemoreceptors are stimulated in response to low oxygen in the blood, rate and depth of
respiration +, px hyperventilates> respiratory alkalosis> vasoconstriction of cerebral
blood vessel= can lead to cerebral hypoxia and ischemia
■ Progressive: if hypoperfusion is not corrected px deterioration begins
● Progressive tissue hypoperfusion, anaerobic metabolism with lactic acidosis> metabolic acidosis,
anaerobic produces less ATP which results in failure of Na/K pump, this leads to cellular edema.
● s/s: dysrhythmia, -BP w/ narrowed pulse, tachypnea, cold, clammy skin, anuria, absent bowel
sounds, lethargy, hyperglycemia, +BUN/creatinine/K, respiratory/metabolic acidosis
■ Refractory: Prolonged inadequate tissue perfusion
● Unresponsive to therapy
● Contributes to multiple organ dysfunction and death
○ Hypovolemic Shock:
■ Causes
● Hemorrhage or severe dehydration, burns
■ Signs and Symptoms
● Increased HR, decreased BP, decreased CVP, skin is cool
● Tachypnea, oliguria, decreased mental status
