Chapter 16
Shock
Learning Objectives
Explain difference between compensated and
uncompensated shock
Differentiate among 5 causes and types of
shock:
Hypovolemic
Cardiogenic
Neurogenic
Septic
Anaphylactic
Learning Objectives
Define rapid responders, transient
responders, and nonresponders
List benefits of packed red blood cell
transfusion
Differentiate among 4 blood types: O, A, B,
Learning Objectives
Demonstrate proper procedure for packed
red blood cell administration for hypovolemic
shock
Learning Objectives
Discuss medications used in treatment of
cardiogenic shock:
Dobutamine (Dobutrex)
Dopamine (Intropin)
Norepinephrine (Levophed)
Milrinone (Primacor)
Learning Objectives
Discuss use of phenylephrine
(Neo-Synephrine) in treatment of neurogenic shock
Explain why, in septic shock, the exaggerated
response, not the infection, creates shock
state
Introduction
Must understand:
What shock is
Causes
Treatments for each particular type
Must recognize:
Condition and know appropriate drug intervention
Presence of condition and determine cause
Overview of Shock
Abnormality of circulatory system
Results in inadequate tissue perfusion and O
2delivery
Impaired O
2delivery can occur in presence of
low, normal, and elevated BP
Do not assume only hypotensive patients can be
in shock
Overview of Shock
Decompensated shock
Presentation of hypotension and tachycardia
occurring in late stages of shock
Patient has lost ability to compensate
Before becoming unstable, patient’s physiologic
functioning alters to compensate
•Normal mentation •Slight alterations in vital signs •Appear stable
Overview of Shock
Early findings:
Skin perfusion
Respiratory rate
Altered mental status
Delayed capillary refill
Cold and clammy skin
Overview of Shock
Respiratory rate can increase to improve
minute ventilation
Compensates for metabolic acidosis
Improves blood return to the heart
•Improved cardiac output
Must maintain high index of suspicion
Signs of shock can be subtle
Overview of Shock
Uncompensated shock
Can be determined quickly
Indicator is perfusion of BP
Can be obtained by palpation of peripheral pulses
Bounding radial pulse indicates patient has
adequate BP of at least 90 mm Hg
Cerebral perfusion can be determined by
Causes of Shock
Hypotension treatment
Administer fluids and vasopressor
If cause is blood loss from GI bleed or MI, blood
flow to vital organs actually decreases despite
normal BP
If patient is in septic shock from perforated colon,
IV fluids and vasopressors do nothing to control
fecal contamination of abdominal cavity
If tension pneumothorax, requires rapid
decompression of the chest
Causes of Shock
Types of shock
Hypovolemic
Cardiogenic
Neurogenic
Septic
Anaphylactic
IV resuscitation is required in all types
Management
Hypovolemic shock
Tachycardic
Prolonged capillary refill and cool extremities
indicates peripheral vasoconstriction
Typically associated with heart rate slower than
expected for degree of hypotension
Drop in BP from acute hemorrhage requires a loss
of approximately 30% of the circulating blood
volume
Management
Hypovolemic shock
Must control source of hemorrhage
Begin fluid resuscitation
•Crystalloid, preferably normal saline
•Ringer lactate solution is used, but it is not compatible with infusion of blood
•IV lines must be flushed with normal saline before blood administration
•Route is optimally two large-bore peripheral IV sites •Rapid bolus of 1 to 2 L of crystalloid
Management
Hypovolemic shock
Rapid responders
•Patients with improved perfusion, heart rate, or BP from crystalloid infusion
•Do not need further aggressive resuscitation •No ongoing hemorrhage
•Source of bleeding controlled with pressure or patient’s normal hemostatic mechanisms
Management
Hypovolemic shock
Transient responders
•Improve as their intravascular volume is replenished •Ongoing manifestations of poor perfusion return •Require blood transfusion and control of hemorrhage
Nonresponders
•Uncontrolled hemorrhage
Management
Hypovolemic shock
Hypotensive resuscitation
•Goal is not to return vital signs to normal, but to maintain physiologic functioning until source of hemorrhage can be controlled
Management
Hypovolemic shock
Administration of IV fluids in excessive amount or
too rapidly can cause patient to bleed more rapidly
•Control of hemorrhage for torso trauma requires rapid access to trauma surgeon
•Saline lacks ability to carry O2and unable to form blood
clots
•Can dislodge clot and cause bleeding to resume •Platelets and coagulation proteins consumed in clot
formations would be lost
•If fluids are not warmed, possible hypothermia occurs
Management
Hypovolemic shock
Must restore systolic BP to subnormal levels, not
normal levels
After control of hemorrhage, standard end points
of resuscitation are sought
Management
Hypovolemic shock
Fluid is administered in volumes to achieve one of
the following results:
•Consciousness, as demonstrated by ability to follow commands
•Palpable radial pulse •Systolic BP of 90 mm Hg •Mean arterial pressure of 60 mm Hg
Management
Hypovolemic shock
May require blood transfusion
•Skill required of air medics, interhospital transport, and military providers
•Blood product most often used: packed red blood cells (pRBCs)
•pRBC transfusion has benefits: O2-carrying capability •Risk: disease transmission
•Risk: ABO-incompatible blood transfusions
Management
Hypovolemic shock
May require blood transfusion
•Blood types: O: universal donor
A: has A antigen on RBC surface B: has B antigen on RBC surface AB: has A and B antigens on RBC surface
•Natural antibodies occur against cell surface antigen that is not present on RBC surface
Management
Hypovolemic shock
May require blood transfusion
•Optimal unit of pRBCs for field administration if type O Rh¯
Rh status is of minimal consequence unless female patient with possibility of future pregnancy Rh¯ patients who receive Rh+blood develop
antibodies against Rh factor in approximately 80% of cases
Management
Hypovolemic shock
Administering blood transfusion
•Equipment needed: 1 U pRBCs Blood tubing Normal saline PPE
Management
Hypovolemic shock
Administering blood transfusion
•Procedure:
Observe universal precautions Confirm right patient
When possible, explain to patient what procedure you are going to perform and why
Examine refrigeration record to ensure proper pRBC temperature has been maintained
Management
Hypovolemic shock
Administering blood transfusion
•Procedure:
Confirm blood type is O
Examine blood for evidence of leakage, clumps, or abnormal color
Confirm the blood is Rh¯ if the patient is a woman younger than 50 years
Record patient vital signs before transfusion and at least every 15 min during transfusion
Ensure all tags and labels remain attached to unit of blood
Management
Hypovolemic shock
Administering blood transfusion
•Procedure:
Ensure tubing to unit of blood is filtered
Confirm pRBCs will be infused through line flushed with normal saline
Attach unit of pRBCs to tubing and open valve to begin transfusion
Closely observe transfusion during first 15 mL of transfusion
Document identifying numbers of unit infused, infusion times, and vital signs
Management
Cardiogenic shock
Inadequate tissue perfusion caused by pump
failure, most commonly from acute MI
Myocardium loses its ability to contract effectively
Factors other than pump failure can result in
cardiogenic shock
Mechanical factors that result in inadequate filling
of right or left atrium can prevent effective cardiac
function
Management
Cardiogenic shock
Blood does not maintain an effective,
unidirectional flow through the heart
•Tissue perfusion is negatively affected
Clinical findings:
•Tissue perfusion manifested by: Peripheral vasoconstriction Delayed capillary refill Decreased mental capacity •Pulmonary congestion •Pulmonary edema
Management
Cardiogenic shock
In acute left ventricular dysfunction, heart is
unable to propel blood to systemic peripheral
circulation
•Lower pressure right ventricle and pulmonary circulation are less affected by pump failure
•Blood flow through right side of the heart to the lungs continues
•In left side of the heart, cardiac emptying to peripheral circulation is compromised
•Left arterial filling pressures increase, resulting in congestion of pulmonary vascular bed
Management
Cardiogenic shock
In acute left ventricular dysfunction, heart is
unable to propel blood to systemic peripheral
circulation
•Tachypnea, shortness of breath, and rales are observed •In acute valvular dysfunction, cardiac murmurs can be
Management
Cardiogenic shock
Mortality rate is between 50% and 80%
Risk factors for death:
•Age •Previous MI •Cold and clammy skin •Oliguria
Best outcomes are in patients when cause of
cardiac dysfunction can be quickly reversed
•Achieved by myocardial revascularization
Management
Cardiogenic shock
In cardiogenic shock caused by cardiac ischemia:
•Nitroglycerin is not indicated
Hypotension can be exacerbated by its vasodilatory effects •Beta adrenergic blockers should be limited
Only used after resolution of the state of hypoperfusion
Management
Cardiogenic shock
Adrenergic agonists can manipulate:
•Heart rate
•Force of cardiac contraction •Systemic vascular resistance
Adrenergic receptor groups:
•Alpha1
•Alpha2
•Beta1
Management
Cardiogenic shock
Dobutamine
•Agent of choice for patients with systolic pressure greater than 80 mm Hg
•Increases cardiac contractility and output •Does not significantly increase heart rate •Does not raise systemic vascular resistance •Must observe for tachycardia and hypotension •Use with caution in atrial fibrillation
Management
Cardiogenic shock
Dopamine
•Beta1-mediated increase in contractility and heart rate
improves cardiac output
•Downside: increases myocardial O2consumption
•Used for cardiogenic shock associated with hypotension •Has beta1and alpha1effects
•Can exacerbate myocardial ischemia from tachycardia and increased systemic vascular resistance
Management
Cardiogenic shock
Norepinephrine
•Used in patients with cardiogenic shock refractory to dopamine
•Is an alpha1, alpha2, and beta1agonist
Management
Cardiogenic shock
Milrinone (Primacor)
•Stimulates heart to increase cardiac output independently of adrenergic receptors •Phosphodiesterase inhibitor
•Used in patients who are nonresponsive to adrenergic stimulating agents
•Has positive inotropic effect and peripheral vasodilatory action
•No significant chronotropic or arrhythmogenic action •Closely observe for hypotension
Management
Cardiogenic shock
When infusing vasoactive medications, monitoring
is critical for:
•Hypoperfusion •Cardiac arrhythmias
•Exacerbation of myocardial ischemia
Management
Cardiogenic shock
Venous access must be maintained and secured
•If IV line becomes dislodged and vasoactive drug infiltrates into soft tissue, may cause soft tissue necrosis at site of infiltration
•Possible soft tissue damage with Sub-Q infusion of adrenergic agonists from an infiltrated site
Management
Neurogenic shock
Possible with spinal cord injury
When sympathetic pathways from spinal cord are
interrupted, blood vessels dilate
•Volume of vascular tree has enlarged but amount of blood filling vasculature has remained the same
Relative hypovolemia occurs
•Lesion to spinal cord involves sympathetic innervations of the heart
•Possible bradycardia
Management
Neurogenic shock
Patients lose input to blood vessels from the
nervous system
•Blood vessels dilate
•Without losing single drop of blood, patient is initially hypovolemic
Management
Neurogenic shock
Fluid infusion to improve preload is initial therapy
Must manage bigger vascular container; fluid
administration refills that vascular container
Do not assume hypotension is from spinal shock
and then use a vasopressor
Management
Neurogenic shock
Treatment for hypotensive trauma: IV fluid therapy
•Use in moderation
•Hypotension from spinal shock may not exhibit expected tachycardia
Management
Neurogenic shock
Vasopressor agents
•Used after the volume status is adequate •Dopamine
Used if patient has low heart rate Possesses alpha effects
Has beta1properties that increase heart rate
Management
Neurogenic shock
Vasopressor agents
•Phenylephrine (Neo-Synephrine) Stimulates only the alpha receptor Most common choice for neurogenic shock
Management
Septic shock
Poor blood perfusion from systemic effects of
infection
Infection localized to blood, lungs, urine, or an
abscess
Body responds to infection by defensive
inflammatory response that is exaggerated
•Exaggerated response, not the infection, creates shock state
Management
Septic shock
Systemic inflammatory response
•Massive inflammatory reaction that produces chaos in several of body’s vital organ systems
•Produces toxins within body that result in dilation of blood vessels
•Blood vessels become “leaky” •Patient can become hypovolemic
Management
Septic shock
Supportive drug therapy
•Intravascular volume expansion with IV fluids •Vasopressors after fluid resuscitation
Norepinephrine Dopamine
