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Critical Care Nuts & Bolts | Lisa Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Shock: Shock States


Module Description
Shock is a term used to include multiple situations and disease processes that result in
tissue hypoperfusion. This module will identify the different types of shock and discuss
the etiology, presentation and management of each.

Module Learning Outcomes


This module prepares the learner to:
1. Discuss the pathophysiology associated with various shock states.
2. Discuss hemodynamic findings and variations found between the different shock
states.
3. Review components of oxygen delivery and extraction through the use of tissueoxygenation monitoring.

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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Shock
The inability of the circulatory system to deliver enough blood to meet the oxygen and nutrient
requirements of body tissues
o Inadequate tissue perfusion can result in:
Generalized cellular hypoxia (starvation)
Widespread impairment of cellular metabolism
Tissue damage
Organ failure
Death
In adults:
o SBP < 90 mm Hg
o MAP < 60 mm Hg
o Decrease in SBP > 40 mm Hg from the patients baseline
Universal conditions with shock
o Hypoperfusion
o Activation of the inflammatory response
o Hypercoagulability
Stages of Shock
Initial stage
o Tissues are underperfused
o Decreased CO
o Increased anaerobic metabolism
o Increased lactic acid
Compensatory stage
o Reversible
o SNS activated by low CO
o Attempting to compensate for the decreased tissue perfusion.
Progressive stage
o Failing compensatory mechanisms
o Profound vasoconstriction from the SNS
o Ischemia
o Lactic acid production high
o Metabolic acidosis
Irreversible, or refractory, stage
o Cellular necrosis
o Multiple organ dysfunction syndrome (MODS)
o Disseminated intravascular coagulation (DIC)
Compensatory Mechanisms
Neural response
o Baroreceptors in aorta and carotids - volume sensitive
o Activate the vasomotor center of the medulla
Hormonal response
o Production of catecholamines (epinephrine and norepinephrine), ACTH
o Renin-angiotensin-aldosterone (RAAS) activation

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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Sympathetic response
o Attempt to maintain stroke volume and BP
o Increase CO/CI initially to compensate
o Then CO/CI decreases
o SVR/SVRI increases
RAAS
o Renin released by juxtaglomerular cells
o SNS stimulation
Decreased blood flow

Hypothalamic pituitary axis


o Cortisol released by adrenal glands
Increases vascular tone
Increases myocardial contractility
o Vasopressin released by posterior pituitary
AKA: Antidiuretic hormone (ADH)
Vasopressin
o Stimulated in response to:
Hypovolemia
Hypotension
MED-ED, Inc. | 1911 Charlotte Dr., Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
Copyright 2015 MED-ED, Inc., All Rights Reserved
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Decreased RV filling
High-serum osmolality
Vasopressin physiology
o Acts on the renal collecting tubules and ducts to reabsorb H20
o This causes more H20 to go back into circulation.
o Less H2O is allowed to form urine, so urine becomes very concentrated.
Vasopressin during shock
o Activates V1 receptors on vascular smooth muscle leading to increased BP
Very strong response if blood volume is 15%-25% less than normal.
o Secretion can increase to greater than 50% of normal levels in order to maintain BP.
Signs of organ hypoperfusion
o Mental status change
o Oliguria
o Lactic acidosis

Cardiac Output
CO = HR x SV (stroke volume)
Determinants of SV
o Preload: increased preload = increased SV. Decreased preload = decreased SV.
o Afterload: inversely proportional to CO. High afterload = low CO. Low afterload = high CO.
o Contractility: increased contractility = increased SV. Decreased contractility = decreased SV.
Preload
o Defined as the amount of fiber stretch before systole
o Measured by CVP
o Starlings law
Increased stretch = increased volume = better ejection
Stretch is within physiological limits
Afterload
o Defined as the resistance to ventricular ejection.
The higher the resistance, the higher the myocardial oxygen demand and workload.
o Vasopressors are used to increase perfusion pressure.
Administered to patients who have failed to respond to fluid administration.
Does not always improve tissue oxygenation despite an increase in blood pressure.
Contractility
o Several different parameters are used to reflect contractility
o Stroke volume (SV)
o Stroke volume index (SVI)
o Left ventricular stroke work index (LVSWI)
o Right ventricular stroke work index (RVSWI)
Types of Shock
Cardiogenic
o Results from ineffective pumping of the heart
Hypovolemic
o Results from insufficient volume of circulating blood
Distributive
o Massive vasodilation of the vascular bed, causing maldistribution of blood
Obstructive
o Decrease blood flow secondary to outflow obstruction
Hypovolemic Shock
Causes
o Major trauma
Blunt or penetrating
o Major burns
o GI fluid loss
Vomiting/diarrhea
MED-ED, Inc. | 1911 Charlotte Dr., Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

NGT decompression
Heat stroke
Massive diaphoresis
Physiology
o Loss of intravascular volume
o Sensed by baroreceptors in aortic arch and carotid bodies
o Activates the neuroendocrine response to stress
Classification of hemorrhagic shock
Treatment
o Isotonic fluid replacement
LR or NS
o If trauma patient, follow Advanced Trauma Life Support (ATLS) guidelines:
2 L crystalloid, give packed red blood cells (PRBCs)
Platelets, cryoprecipitate, FFP as needed
o Monitor electrolytes and lactate
o

Cardiogenic Shock
Causes
o Most commonly occurs after ST-segment elevation myocardial infarction (STEMI)
Mortality 56%-67%
Inadequate tissue perfusion/oxygenation caused by cardiac dysfunction
Usually decreases in LV contractility
On autopsy > 40% loss of LV muscle
o Cardiomyopathies
o Trauma
o Acute aortic/mitral valve regurgitation
o Acute aortic/mitral stenosis
o Ventricular septal defect
o LV wall rupture
o Myocarditis
Decreased supply
o Spasms
Decreased coronary perfusion
Decreased blood O2

Stenosis or thrombus
o Increased demand
Increased HR
Increased contractility
Increased LV-wall tension
o Pathophysiology
Sympathetic nervous system
Increases myocardial O2 demand
Can worsen myocardial ischemia
Renin-angiotensin system
Increased preload
Increased afterload
Cellular level
Ischemia leads to anaerobic metabolism
Lactate buildup causes intracellular acidosis
Myocyte transport pumps fail:
o Na+ & Ca+ accumulate
o Myocytes swell myocyte overstretch
o Inflammatory cascade initiated, oxidative injury occurs
o Can lead to cell death (apoptosis) around the area of infarction
o If ischemia is severe or prolonged:
Irreversible cell injury
MED-ED, Inc. | 1911 Charlotte Dr., Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Myocyte necrosis
Diastolic dysfunction
Systolic dysfunction
Management
o Optimizing preload
o Hypervolemia
Diuretics
Vasodilators
Nitroglycerin
Morphine
o Optimizing afterload
High afterload
Arterial vasodilators
AV replacement
Treat the shock
o Optimizing contractility
Positive ionotropes
Reverse ischemia
Valve surgery
Biventricular pacer

Obstructive Shock
Hypodynamic shock state
o Decreased blood flow secondary due to outflow obstruction
Increased filling pressures
Impaired ventricular filling and decreased ventricular compliance
o Causes
Pericardial tamponade
Tension pneumothorax
Acute pulmonary embolism
o Treatment
Correct source of outflow obstruction
Needle decompression for PTX
Pericardiocentesis for tamponade
Antithrombolytics for pulmonary embolism
o Pericardial tamponade
Physical findings
Distended neck veins
Increased CVP
Pulsus paradoxus
Decreased cardiac output
Hypotension that does not respond to fluid bolus (Becks triad)
Diminished heart sounds
Tachycardia
Diagnosis
Echocardiogram
FAST (focused assessment with sonography for trauma)
Lab studies
o CPK, chemistry, coagulation studies
o Chest X-ray
o 12-Lead ECG
o Hemodynamic monitoring

Treatment
Pericardiocentesis with echo guidance should be performed as soon as diagnosis made
Oxygen/ventilatory support if indicated
MED-ED, Inc. | 1911 Charlotte Dr., Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
Copyright 2015 MED-ED, Inc., All Rights Reserved
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Inotropic support (dobutamine)


Volume expansion to restore intravascular volume if needed
Distributive Shock
Physiology
o Maldistribution of blood flow/volume
Oxygen extraction is normal or decreased despite hypoperfusion.
Refractory hypotension despite adequate fluid
o Systemic effects of cytokines
Causes
o Sepsis
Widespread inflammation with infection
o Multiple organ dysfunction syndrome
Organs affected: brain, lungs, kidneys, hepatobiliary, GI, coagulation, CV
Initial resuscitation
o Protocolized, quantitative resuscitation of patients with sepsis induced hypoperfusion
Hypotension after initial fluid challenge or lactate > 4 mmol
Within 6 hours, achieve CVP 8-12 mm Hg
MAP > 65 mm Hg
U/O > 0.5 mL/kg/hr
ScVO2 > 70% or SVO2 >65% (1C)
Target resuscitation to normalize lactate level (2C)
Antimicrobial therapy
o Administration of effective antimicrobials within the first hour of recognition of septic shock
(1B) and within 3 hours of severe sepsis without septic shock (1C)
Each hour delay in antibiotic increases mortality by 5%
Selection of empiric therapy
Procalcitonin only for antibiotic stewardship
Combination empirical therapy
Markers of shock
o Lactate
Widely used method of determining tissue oxygen balance
Lactate > 2 mEq/L are abnormal
o Base deficit
On ABG, base deficit
> -5 is indicative of decreased tissue perfusion or shock
o Maintain adequate tissue oxygenation
o The adequacy of tissue oxygenation is determined by how much oxygen is delivered to the
tissues versus how much oxygen is required to sustain aerobic metabolism.
Global tissue hypoxia

MED-ED, Inc. | 1911 Charlotte Dr., Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net


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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Practice Questions
1. Shock is best described as which of the following?
a.
b.
c.
d.

a decrease in blood pressure


occurs due to loss of blood volume
inadequate tissue oxygenation
involves the parasympathetic nervous system

2. Which of the following hemodynamic parameters would be an alert to the ICU nurse that the patient
may be in shock?
a.
b.
c.
d.

systolic blood pressure (SBP) < 90 mm Hg


mean arterial pressure (MAP) of 70
heart rate of 80
decrease SBP from 160 to 140 mm Hg

3. Which of the following physiological changes commonly accompanies shock?


a.
b.
c.
d.

aerobic metabolism
hypercoagulable state
decrease in lactic acid
activation parasympathetic nervous system

4. A patient has a decrease in his or her cardiac output (CO). The ICU nurse notes the patients heart
rate is elevated and blood pressure remains normal. Which of the following stages of shock is this
patient currently in?
a.
b.
c.
d.

early shock
compensated shock
progressive shock
refractory shock

5. The following lab work is obtained on a patient in shock: WBC: 14,000, pH 7.20, bicarbonate 12, lactic
acid 6 mmol/L. Which of the following stages of shock would you expect this patient to be
experiencing?
a.
b.
c.
d.

early shock
compensated shock
progressive shock
refractory shock

6. The patient has developed acute kidney injury and hepatic failure following a period of tissue
hypoperfusion. This patient would be considered a refractory shock.
a. true
b. false
7. Which of the following findings would indicate the stimulation of the rein-angiotensin-aldosterone
system (RAAS) in response to a decrease in cardiac output or shock?
a.
b.
c.
d.

diaphoresis
increase in respiratory rate
increase in heart rate
decrease in urine output

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net


Copyright 2015 MED-ED, Inc., All Rights Reserved.
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Practice Questions
8. Vasopressin is released during shock to increase reabsorption of water in the renal collecting ducts.
Where is vasopressin released from?
a.
b.
c.
d.

the
the
the
the

hypothalamus
adrenal glands
posterior pituitary
pancreas

9. Which of the following statements best describes stroke volume?


a. the amount of blood that leaves the heart in 1 minute
b. the percentage of blood that leaves the heart compared to the amount remaining in the
heart per contraction
c. the amount of blood that leaves the heart per contraction
d. the stretch on the heart before the contraction
10. Which of the following is the term used for the resistance the ventricle has to eject against?
a.
b.
c.
d.

preload
contractility
afterload
ejection fraction

11. Shock that is caused by massive vasodilation of the vascular bed and maldistribution of blood is
called:
a.
b.
c.
d.

cardiogenic shock
hypovolemic shock
distributive shock
obstructive shock

12. A patient has been vomiting for the past 24 hours and is now hypotensive and tachycardic. The
physician states that the patient is in hypovolemic shock. Which of the following IV fluids would the
ICU nurse expect the physician to order initially?
a.
b.
c.
d.

fresh frozen plasma


D5NS
D5W
normal saline

13. Which of the following is the most common cause of cardiogenic shock?
a.
b.
c.
d.

acute mitral regurgitation


trauma
acute myocardial infarction (AMI)
congestive heart failure

14. Following a blunt chest trauma, the victim develops a severe pericardial tamponade and shock. Which
of the following types of shock would the patient most likely be experiencing?
a.
b.
c.
d.

cardiogenic shock
distributive shock
hypovolemic shock
obstructive shock
MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
Copyright 2015 MED-ED, Inc., All Rights Reserved.
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Answers
1. C
Rationale: Shock is best described as a decrease in tissue oxygenation caused by poor tissue perfusion. A
loss of blood volume (hypovolemia) can cause shock but is not the only cause of shock. Shock can involve
a decrease in blood pressure but tissue hypoperfusion can occur even with a normal blood pressure.
Shock does not involve the parasympathetic nervous system.
2. A
Rationale: A systolic blood pressure less than 90 mmHg may indicate shock and should be monitored
closely. The other options are considered normal vital sign findings.
3. B
Rationale: When the proinflammatory cytokines are released in shock (tissue hypoperfusion), they initiate
the coagulation system. A hypercoagulable state is a universal finding of shock along with an
inflammatory response. Patients in shock will be in an anaerobic metabolism, not an aerobic. There is an
increase in lactic acid, not a decrease, and the sympathetic nervous system is activated, not the
parasympathetic.
4. B
Rationale: Early shock is accompanied by a decrease in cardiac output, but the bodys compensatory
mechanisms of tachycardia and vasoconstriction will allow assistance with maintaining tissue perfusion.
This is called compensated shock. The patient in this example is tachycardic and currently has a normal
blood pressure. Those are signs of compensation during periods of decreased CO. Progressive shock is
when the compensatory mechanisms fail and the tissue hypoxia worsens. Refractory shock is the endresult of tissue hypoperfusion and is characterized by multisystem organ failure.
5. C
Rationale: Progressive shock occurs when the compensatory mechanism fails and is characterized by
extreme metabolic acidosis (pH 7.20 with lactic acid of 6 mmol/L). The question did not provide any lab
work demonstrating multisystem organ failure, so this would not have been considered a refractory shock
at this time.
6. A
Rationale: Refractory shock is prolonged ischemia resulting in cellular death and is characterized as
multisystem organ failure (acute kidney injury and hepatic failure).
7. D
Rationale: RAAS is a compensatory system for shock. It is initiated by a decrease in CO and renal
hypoperfusion. The release of aldosterone causes the kidneys to reabsorb sodium and water (thus
decreasing the urine output) to increase circulating blood volume. The activation of the sympathetic
nervous system causes the diaphoresis, increased respiratory rate and tachycardia.
8. C
Rationale: Vasopressin is produced in the hypothalamus, but is stored and released from the posterior
pituitary. Situations of hypovolemia and hyperosmolar states trigger the release of vasopressin from the
posterior pituitary. The adrenal glands produce cortisol, which also occurs during shock. The pancreas
releases insulin.
MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net
Copyright 2015 MED-ED, Inc., All Rights Reserved.
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Shock: Shock States | Lisa M. Soltis, MSN, APRN, PCCN, CCRN-CSC, CCNS, FCCM

Answers
9. C
Rationale: Stroke volume (SV) is the amount of blood that leaves the heart per contraction. The cardiac
output (CO) is the amount that leaves the heart per minute. The CO can be calculated by multiplying the
SV times the heart rate. The percentage of blood that leaves the heart compared to the amount remaining
in the heart per contraction is the ejection fraction. The stretch on the heart before the onset of systole
(contraction) is called the preload.
10. C
Rationale: Afterload is the resistance to ventricular ejection. The higher the resistance, the lower the
cardiac output (CO). Preload is the volume in the ventricles at the end of diastole. Contractility is the force
of recoil allowing for greater CO. Ejection fraction is used to measure contractility.
11. C
Rationale: Distributive shock is the term used to describe shock states that are a result of massive
vasodilation and maldistribution of blood flow causing tissue hypoperfusion. Septic shock is an example of
distributive shock. Cardiogenic shock is a result of an ineffective pump. Hypovolemic shock is caused by
insufficient volume of circulating blood. Obstructive shock is a decrease blood flow secondary to outflow
obstruction.
12. D
Rationale: Normal saline and lactated ringers are isotonic solutions that are used to resuscitate vascular
losses in hypovolemic shock. Fluids given to replace vascular losses should be isotonic and without
glucose. D5W is hypotonic, and D5NS contains glucose. Fresh frozen plasma would not be indicated
initially unless the patient was noted to have a high INR.
13. C
Rationale: AMIs resulting in ischemia/infarction of the ventricular wall affect the contractility. This leads
to severe heart failure and an inability to pump. Trauma, acute mitral regurgitation and congestive heart
failure are all potential causes of cardiogenic shock but are not as common.
14. D
Rationale: Pericardial tamponade produces an obstructive shock. The blood is unable to enter the
ventricle to adequately fill the ventricle and is unable to leave due to the obstruction of the blood filled
pericardial sac. This results in a significant decrease in cardiac output and shock. Hypovolemic shock
may accompany the pericardial tamponade because the patient was a trauma, but there is not any
indication of other injuries in the scenario to indicate significant blood loss. It is not from lack of
ventricular contractility but from obstruction, so it would not be cardiogenic shock. It is not associated
with vasodilation, so would not be classified as distributive shock.

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net


Copyright 2015 MED-ED, Inc., All Rights Reserved.
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