Download 2-25-2009 SHOCK FINAL

SHOCK
SHOCK
ADULT HEALTH II
SPRING, 2009
Jerry Carley
MSN, MA, RN, CNE
January 2009:
Brazilian Super Model Dies
Questions
To
Ponder:
Shock
• 1. A client arrives in the emergency room in the
nonprogressive stage of shock. What clinical
manifestations would the nurse expect this client to
exhibit?
•
•
•
•
A.
B.
C.
D.
Decreased heart rate and decreased urinary output
Increased heart rate and decreased urinary output
Increased pulse pressure and increased heart rate
Decreased pulse pressure and decreased heart rate
• 2. Your client has multi-trauma & just arrived in
the ER. The client’s urinary output is normal,
whereas respiratory rate and heart rate are
slightly elevated from baseline. Which of the
following should the nurse suspect?
•
•
•
•
A.
B.
C.
D.
Early stage of shock
Compensatory stage of shock
Intermediate stage of shock
Refractory stage of shock
• 3. A client has been admitted with a
gastrointestinal ulcer. The client is NPO and has
a nasogastric tube in place connected to low
intermittent suction. What form of shock should
the nurse suspect / monitor this client for?
•
•
•
•
A.
B.
C.
D.
Distributive shock
Obstructive shock
Cardiogenic shock
Hypovolemic shock
• 4. A client brought to the emergency room
after a motor vehicle accident is suspected of
having internal bleeding. What initial clinical
manifestation of hypovolemic shock would
the nurse expect to find in this client?
•
•
•
•
A.
B.
C.
D.
Increased respiratory rate
Decreased urinary output
Increased heart rate
Cool, pale skin
• 5. A client in hypovolemic shock has been
placed on a dopamine hydrochloride drip.
Which parameter would indicate a desired
client response to this drug?
•
•
•
•
A.
B.
C.
D.
Hypotension
Tachycardia
Increased cardiac output
Decreased mean arterial pressure
• 6. A nurse is monitoring a client who is
receiving a dopamine hydrochloride drip for
the treatment of shock. What symptom
would indicate a possible overdose of this
medication?
•
•
•
•
A.
B.
C.
D.
Pallor
Hypertension
Palmar erythema
Increased pulse deficit
• 7. What assessment is most appropriate for
the client receiving sodium nitroprusside?
•
•
•
•
A. Assess for chest pain.
B. Assess blood pressure every 15 minutes.
C. Monitor urinary output every 30 minutes.
D. Observe the client’s extremities for color
and perfusion.
• 8. Which manifestations should the nurse
expect when caring for the client with
distributive shock resulting from an anaphylactic
event?
•
•
•
•
A.
B.
C.
D.
Increased heart rate and blood pressure
Increased blood pressure and cardiac output
Decreased blood pressure and respiratory rate
Decreased blood pressure and edema
• 9. The client has all the following clinical
manifestations. Which one alerts the nurse to
the probability of septic shock?
•
•
•
•
A.
B.
C.
D.
Hypotension
Pale, clammy skin
Anxiety and confusion
Oozing of blood at the IV site
• 10. The average blood volume for an adult is
65 – 75 mL /Kg
• The client weighs 209 lbs
• What is the estimated blood volume for this
patient?
End of Quiz
(answers later)
At the conclusion of this presentation,
the nurse will be able to:
• 1. Define the concept known as SHOCK.
• 2. Name, discuss, compare and contrast the four general
categories of shock.
• 3. Name, discuss, compare and contrast the four stages of shock.
• 4. Name, discuss, compare and contrast etiology / risk factors
associated with the four general categories of shock.
• 5. Name the various diagnostic tests helpful in diagnosing and
monitoring shock.
• 6. Identify and Discuss nursing interventions associated with
treatment of clients with shock
• 7. Identify and Discuss the stages of shock; compare and contrast
associated assessment findings with the stages of shock.
• 8. Identify and discuss pharmacologic medications and
interventions associated with the various types of shock.
• C.O.
•
•
= HR X SV
(CRAP)
contractility rate afterload preload
• BP= C.O.
X PVR
• MAP= (2 x D) + S / 3
A Concept Map: Shock
Hypovolemic Shock
NSG DX
Insufficient oxygenation of tissues
related to a sustained decrease in
mean arterial pressure (MAP)
Seth, 17 y.o.
Multi-Trauma
Decreased
Cardiac
Output
Risk Factors
Cardiovascular:
Medical History: Negative
Medications:
None
Lab Studies:
Hgb 12.2
Hct 55%
WBC 18.8
BS 110
Physical Exam:
HR 138
Resp 32
BP 88/68
Pulse Ox 85%
Restless, Irritable
Respiratory:
Tachypnea (+)
Lungs CTA
Integumentary:
Pallor (+)
Capillary Refill > 3 sec
Risk for
Ineffective
Tissue
Perfusion
CNS:
Deficient
Fluid
Volume
Change in level of
consciousness
Pain, acute
Glasgow= 10
Musculoskeletal:
Deformity, ecchymosis
and edema, both thighs
Deformity, ecchymosis,
crepitance bilat lower rib
cage
Cardiac /
Pump
Effectiveness
F/E
Management
Circulation
Status
IV
Therapy
Kidney / Urinary:
Output < 30 mL/hr
SG > 1.035
Hemodynamic
Regulation
PATIENT
Outcomes
Shock
Management
Tachycardia (+)
Hypotension (+)
Decreased PO2 (+)
analyze
*Chief Complaint: S/P
MVC
Pain
Multiple Fractures
Lower Extremities;
Fractured lower two
ribs, bilateral
NURSING
Interventions
Pain
Fluid
Balance
Hypovolemia
Management
Pain
Management
Immobilization /
Pain Medications
A Tale of
4 Patients
Boyd, 17 y.o.
S/P MVA,
Multiple Trauma
Hypovolemic
Shock
Obstructive
Shock
Roseline, 36 y.o. w/ hx
Aortic Stenosis, CHF
Frank 32 y.o.
Anaphylaxis
Septic
Shock
Distributive
Shock
Ian, 26 y.o.
Meningococcal meningitis
Defined…
• Shock: a state of inadequate tissue perfusion
that impairs maintenance of normal cellular
metabolism. Any condition that compromises
oxygen delivery to tissues and organs can
STAGES:
INITIAL
cause shock.
COMPENSATORY
PROGRESSIVE,
REFRACTORY
THE CAUSE OF SHOCK,
CATEGORY OF SHOCK,
AND STAGE OF SHOCK
DIRECT THE SPECIFIC TREATMENT
Types of Shock
(Classified by underlying cause)
•Cardiogenic
•Hypovolemic
•Distributive
•Obstructive
“Pump Failure” or “Heart Failure”
Decrease in intravascular volume
of 10-15% or more
Widespread vasodilation and capillary
permeability (3 types…)
(septic, neurogenic, anaphylactic)
Mechanical blockage in the heart or
great vessels
Progression of Shock (Stages)
Initial
Compensatory
Progressive
Refractory
No visible changes in client parameters, changes are now
occurring on the cellular level only
Body is mounting measures to increase cardiac output to
restore tissue perfusion and oxygenation.
Compensatory mechanisms begin to fail
IRREVERSIBLE;
TOTAL BODY FAILURE
Risk Factors
• Cardiogenic
• Hypovolemic
• Distributive
•
Septic
•
Neurogenic
•
Anaphylactic
• Obstructive
Pump failure due to myocardial infarction, heart failure,
Cardiomyopathy, dysrhythmias, cardiac tamponade,
valvular rupture or valvular stenosis
Excessive fluid loss from diuresis, vomiting & diarrhea;
Blood loss secondary to surgery, trauma, ob-gyn causes;
Burns; Diabetic Ketoacidosis
Endotoxins and other mediators causing massive
vasodilation. Most common is gram-negative bacteria.
Loss of sympathetic tone causing massive
vasodilation. Trauma, spinal shock, and epidural
anesthesia are among the causes.
Antigen-antibody reaction causing massive vasodilation.
Blockage of great vessels. Cardiac valve stenosis, pulmonary
Embolism, and aortic dissection are among the causes.
Diagnostic Procedures
• ABG’s
• Hemodynamic Monitoring
• Cardiogenic Shock:
•
EKG, Echocardiogram, CT Scans, Cardiac catheterization, CXR, Cardiac
Enzymes
• Hypovolemic Shock:
•
Hgb & Hct; Type & Crossmatch; investigate for source of bleeding
• Septic Shock:
•
Cultures: blood, urine, wound
•
Coagulation tests: PT, PTT, INR
• Obstructive Shock:
•
Echocardiogram, CT scan,
• Monitor Signs & Symptoms
•
Hypoxia
•
Hypotension (MAP < 60 mm Hg)
•
Tachycardia, weak thready pulse
Stages of Shock With Associated Assessment Changes
Stage>>>>>>>>
Initial
Compensatory
Progressive
Refractory
Heart Rate
(bpm)
< 100
>100
>120
>140
Systolic BP
normal
Normal/
increased
70-90 mm
Hg
< 50-60 mm Hg
Respiratory Rate
Normal
20-30
30-40
> 40
Urine Output
(mL/hr)
> 30
20-30
5-20
Negligible
Skin
Cool, pink, dry
Cool, pale, dry or
moist
Cold, pale,
moist
Cold, mottled,
Cyanotic, dry
Capillary Refill
Normal
Slightly delayed
Delayed
Not noted
-Miscellaneous: May see rashes with septic or anaphylactic shock.
-May see angioedema with anaphylactic shock.
-Rales (coarse crackles) are possible with cardiogenic shock.
-SEIZURES MAY OCCUR WITH ALL FORMS OF SHOCK.
-FEVER MAY OCCUR WITH ALL FORMS OF SHOCK—
BUT ESPECIALLY SEPTIC SHOCK
Skin Assessment
Shock Position
Evidence-Based Practice
Update:
Friedrich
Trendelenberg
Assess & Monitor
•
•
•
•
•
•
OXYGENATION
PRIORITY: ______________
Vital signs
Urinary Output
LOC
Cardiac Rhythm
Skin color, temperature, moisture, capillary refill,
turgor
• Symptoms related to system:
•
chest pain, change in heart sounds, lung
sounds, bowel sounds, neurological status
NANDA’s
• Decreased Cardiac Output
• Impaired Gas Exchange
• Ineffective Tissue Perfusion
• Deficient Fluid Volume
• Anxiety
Cardiogenic Shock
• When thinking about the hemodynamics of
cardiogenic shock, keep it simple:
• The components of cardiac output are:
Contractility, Rate, Afterload, and Preload, or
“CRAP.” To manage these patients, you’ve got to
know CRAP! (This acronym has long been passed
down to many a critical care and cath lab staff
and is helpful when managing cardiogenic shock).
• Every therapeutic intervention is aimed towards
improving or altering a component of cardiac
output — or something in CRAP.
Nursing Interventions
IDENTIFY CLIENTS AT RISK FOR DEVELOPING
SHOCK BASED UPON RISK FACTORS !
IF SHOCK IS SUSPECTED:
1. Obtain VS, including pulse oximetry
2. Obtain laboratory & diagnostic work
per protocol that will help identify cause
of shock
3. Calculate Urine Output & monitor
hourly urine output. Report U.O. < 30 mL
PLACE CLIENT ON HIGH FLOW OXYGEN,
E.G., 100% NONREBREATHER MASK.
IV ACCESS ! Large Bore IV Catheter(s)
-Position: Flat w/ Legs Elevated or
Trendelenberg Position
-Hemodynamic Monitoring
-Cardiac Monitoring
Pharmacology & Shock
HYPOVOLEMIC
CARDIOGENIC
ANAPHYLACTIC
Volume
Replacement
Colloids &
Crystalloids
Afterload
reducers
Vasopressors
Inotropic
to increase
Agents
blood pressure
(Replace
volume first)
Vasopressors
NEUROGENIC
ALL TYPES
Antihistamines Antibiotics
Volume
Replacement
Proton
Pump
Inhibitors
Epinephrine
Norepinephrine
DVT
Prophylaxis
SEPTIC
Norepinephrine
Heparin,
Then
clotting
factors,
platelets, &
plasma
MAP Mean Arterial Pressure
PT’s BP = 100/60 mm Hg
• MAP = [(2*D)+S] / 3
• [ (2 x 60) + 100] / 3 = 73.3 mm Hg
• It is believed that a MAP that is greater than 60 mmHg is enough to
sustain the organs of the average person.
• If the MAP falls significantly below this number for an appreciable time,
the end organ will not get enough blood flow, and will become ischemic.
Hypovolemic Shock
BACK !
• Average Blood Volume = 65-75 mL /kg
• 75 ml/Kg X 75 kg = 5625 mL = 5.625 L
EBL 10% - 15%
Yields Hypovolemic Shock
0.10 x 5625 = 560 mL
0.15 x 5625 = 844 ml
5-6 Liters
Shock
Pharmacology:
“Pressor Agents”
Milrinone / Amrinone
• Belong to new class of agents “Bipyridines”
• Non-receptor mediated activity based on
selective inhibition of Phosphodiesterase Type
III enzyme resulting in cAMP accumulation in
myocardium
• cAMP increases force of contraction and rate
and extent of relaxation of myocardium
• Inotropic, vasodilator and lusotropic effect
•
( lusotropic= direct improvement of the relaxation phase of the LV.)
Amrinone
(Inacor®)
• First generation agent - limited use now
• Long half-life (4.4 hours) with potential for
prolonged hypotension after loading dose
• Associated with thrombocytopenia
• Dosage: Load with 0.75 mg/kg with infusion
rate of 5-10 mcg/kg/min
• Milrinone is preferred drug from this group
Milrinone
(Primacor®)
• Increases CO by improving contractility,
decreased SVR, PVR , lusotropic effect;
decreased preload due to vasodilatation
• Unique in beneficial effects on RV function
• Half-life is 1-2 hours
• Load with 50 mcg/kg over 30 mins followed by
0.3 to 0.75 mcg/kg/min
• No increase in myocardial O2 requirement
Epinephrine
Actions are dose dependent (mcg/kg/min):
0.02-0.08 = mostly beta1 and beta2 stimulation.
increased cardiac output
mild vasodilation
0.1-2.0 = mix of beta1 and alpha1
increase cardiac output
increase SVR = vasoconstriction
> 2.0 = mostly alpha1
increase SVR, and may decrease CO by
increasing afterload
Dopamine
• Intermediate product in the enzymatic
pathway leading to the production of
norepinephrine; thus, it indirectly acts by
releasing norepinephrine.
• Directly has alpha, beta and dopaminergic
actions which are dose-dependent.
• Indications are based on the adrenergic
actions desired.
Dopamine
• Improve renal perfusion 2-5 mcg/kg/min
• Improve C.O. in mild to moderate Cardiogenic
or Distributive Shock 5-10mcg/kg/min
• Post-resuscitation stabilization in patients with
hypotension (in conjunction with fluid
therapy) 10-20mcg/kg/min
Venodilators / Vasodilators
Classified by site of action
-Venodilators: reduce preload - Nitroglycerin
-Arteriolar dilators: reduce afterload
Minoxidil and Hydralazine
-Combined: act on both arterial and venous
beds and reduce both pre- and afterload
Sodium Nitroprusside (Nipride)
Nipride ®
nitroprusside
-Vasodilator that acts directly on arterial
and venous vascular smooth muscle.
-Indicated in hypertension and low cardiac
output states with increased SVR.
-Also used in post-operative cardiac surgery
to decrease afterload on an injured heart.
-Action is immediate; half-life is short;
titratable action.
Nipride ®
-Toxicity is with cyanide, one of the metabolites
of the breakdown of nipride.
-Severe, unexplained metabolic acidosis might
suggest cyanide toxicity.
-Dose starts at 0.5 mcg/kg/min and titrate to 5
mcg/kg/min to desired effect. May go higher (up
to 10 mcg/kg/min) for short periods of time.
Nitroglycerin
• Direct vasodilator as well, but the major effect
is as a venodilator with lesser effect on
arterioles.
• Not as effective as nitroprusside in lowering
blood pressure.
• Another potential benefit is relaxation of the
coronary arteries, thus improving myocardial
regional blood flow and myocardial oxygen
demand.
NTG
-Used to improve myocardial perfusion following
cardiac surgery
-Dose ranges from 0.5 to 8 mcg/kg/min. Typical
dose is 2 mcg/kg/min for 24 to 48 hours postoperatively
-Methemoglobinemia is potential side effect
Isoproterenol
(Isuprel ®)
-Synthetic catecholamine
-Non-specific beta agonist with minimal alphaadrenergic effects.
-Causes inotropy, chronotropy, and systemic
and pulmonary vasodilatation.
-Indications: bradycardia, decreased cardiac
output, bronchospasm (bronchodilator).
-No longer available in some markets
Isoproterenol
-Occasionally used to maintain heart
rate following heart transplantation.
-Dose starts at 0.01 mcg/kg/min and
is increased to 1.0 mcg/kg/min for
desired effect.
Selecting inotropic and vasopressor agents for specific hemodynamic disturbances
BP or SVR>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Normal
Decreased
Elevated
Hemodynamic
pattern
Septic Shock
Stroke index High
Stroke Index low to N
None or dopamine
Dobutamine or
dopamine
Norepinephrine
Dopamine or epinephrine
(or dobutamine plus
norephinephrine)
Cardiogenic shock
Dobutamine or
amrinone
or dopamine
Epinephrine or dopamine
Myocardial dysfunction
(complicating critical
illness)
Dobutamine or
dopamine
or amrinone
Epinephrine or dopamine
(or dobutamine plus
norepinephrine)
CHF
Dobutamine or
dopamine
or amrinone
Bradycardia
None
None
Dobutamine
plus
nitroprusside
Dobutamine
plus
nitroprusside
Dobutamine
plus
nitroprusside
Isoproterenol
None
• 1. A client arrives in the emergency room in the
nonprogressive stage of shock. What clinical
manifestations would the nurse expect this client to
exhibit?
•
•
•
•
A.
B.
C.
D.
Decreased heart rate and decreased urinary output
Increased heart rate and decreased urinary output
Increased pulse pressure and increased heart rate
Decreased pulse pressure and decreased heart rate
In the nonprogressive stage of shock, both kidney and cardiovascular
compensations, in addition to chemical compensatory mechanisms, are needed.
These result in an increase in heart rate and decrease in urinary output to
maintain MAP (mean arterial pressure) and volume in the central blood vessels.
• 2. Your client has multi-trauma & just arrived in
the ER. The client’s urinary output is normal,
whereas respiratory rate and heart rate are slightly
elevated from baseline. Which of the following
should the nurse suspect?
•
•
•
•
A.
B.
C.
D.
Early stage of shock
Compensatory stage of shock
Intermediate stage of shock
Refractory stage of shock
An increase in heart and respiratory rates (heart rate first) from
the client’s baseline or a slight increase in diastolic blood
pressure may be the only objective manifestations of early
shock.
• 3. A client has been admitted with a
gastrointestinal ulcer. The client is NPO and has a
nasogastric tube in place connected to low
suction. What form of shock should the nurse
monitor this client for?
• A. Distributive shock
• B. Obstructive shock
• C. Cardiogenic shock
• D. Hypovolemic shock
This client is at risk for hypovolemic shock caused by
bleeding from gastrointestinal ulcers, leading to fluid
volume loss, and from nasogastric suction that can
compound the situation if the client is not sufficiently
hydrated with IV fluids.
• 4. A client brought to the emergency room after
a motor vehicle accident is suspected of having
internal bleeding. What initial clinical
manifestation of hypovolemic shock would the
nurse expect to find in this client?
• A. Increased respiratory rate
• B. Decreased urinary output
• C. Increased heart rate
• D. Cool, pale skin
The first manifestations of hypovolemic shock result from
compensatory mechanisms. Signs of shock are first evident as
changes in cardiovascular function. As shock progresses,
changes in skin, respiration, and kidney function progress.
• 5. A client in hypovolemic shock has been
placed on a dopamine hydrochloride drip.
Which parameter would indicate a desired
client response to this drug?
• A. Hypotension
• B. Tachycardia
• C. Increased cardiac output
• D. Decreased mean arterial pressure
Dopamine hydrochloride causes vasoconstriction that, in turn,
increases cardiac output and mean arterial pressure, thereby
improving tissue perfusion and oxygenation.
• 6. A nurse is monitoring a client who is
receiving a dopamine hydrochloride drip for
the treatment of shock. What symptom would
indicate a possible overdose of this
medication?
• A. Pallor
• B. Hypertension
• C. Palmar erythema
• D. Increased pulse deficit
An overdose of dopamine hydrochloride is
manifested by hypertension.
• 7. What assessment is most appropriate for
the client receiving sodium nitroprusside?
• A. Assess for chest pain.
• B. Assess blood pressure every 15 minutes.
• C. Monitor urinary output every 30 minutes.
• D. Observe the client’s extremities for color
and perfusion.
The client receiving sodium nitroprusside should have
his or her blood pressure assessed every 15 minutes.
Higher doses can cause systemic vasodilation and
increase shock.
• 8. Which manifestations should the nurse
expect when caring for the client with distributive
shock resulting from an anaphylactic event?
• A. Increased heart rate and blood pressure
• B. Increased blood pressure and cardiac output
• C. Decreased blood pressure and respiratory rate
• D. Decreased blood pressure and edema
Anaphylaxis damages cells and causes release of large
amounts of histamine and other inflammatory
chemicals, which results in massive blood vessel
dilation and increased capillary leak.
• 9. The client has all the following clinical
manifestations. Which one alerts the nurse to
the probability of septic shock?
• A. Hypotension
• B. Pale, clammy skin
• C. Anxiety and confusion
• D. Oozing of blood at the IV site
The late phase of sepsis-induced distributive shock is characterized by
most of the same cardiovascular manifestations as any other type of
shock. The distinguishing feature is the lack of ability to
clot blood, causing the client to bleed from areas of
minor trauma and to bleed spontaneously.
• 10. The average blood volume for an adult is
65 – 75 mL /Kg
• The client weighs 209 lbs
• What is the estimated blood volume for this
patient?
(209 lbs /2.2 lbs/kg) = 95 kg
65 mL/Kg x 95 kg = 6175 ml
75 mL/kg x 95 kg = 7125 mL
Estimated Blood Volume = 6175-7125 mL
or
6.175 L – 7.125 L
•Reading /
Resources
Cardiogenic Shock and Hemodynamic Support: A Realistic Management Approach
- Mary Dahling, RN, MSN, CCRN, CNS, Cardiothoracic Surgery, Sentara Norfolk Hospital,
Norfolk, Virginia
•
What is cardiogenic shock?
By definition, cardiogenic shock is decreased cardiac output and
evidence of tissue hypoperfusion in the presence of adequate
intravascular volume.1 The presence of adequate intravascular volume is
important. This differentiates cardiogenic shock from other types of shock,
which typically have a relative or an absolute volume deficit. With
cardiogenic shock, the patient usually has enough intravascular volume —
it’s just not going to the right place(s) due to pump failure. These patients
present with sustained hypotension defined by blood pressure less than
80 mmHg (or 90 mmHg if on pressors, inotropic agents or intraaortic
balloon pump support) for greater than 30–60 minutes, a cardiac index
under 1.8 liters/ minute, in the presence of a left ventricular end-diastolic
pressure (LVEDP) or pulmonary capillary wedge pressure (PCWP) greater
than or equal to 18 mmHg.4,5 When dealing with “cardiogenic shock,”
think “decreased forward flow” because interventions must be aimed
toward restoration of forward volume flow. We lose if we don’t perfuse!
Cath Lab Digest - ISSN: 1073-2667 - Volume 11 - Issue 11 - November 2003 - Pages: 20 25
• What causes cardiogenic shock?
The major cause of cardiogenic shock is ischemic disease, both of the
left and right ventricle. Valvular heart disease/dysfunction may also result
in cardiogenic shock, a classic example being acute mitral insufficiency or
regurgitation. Additional causes include:
1. Trauma from a myocardial contusion;
2. Cardiomyopathies: Hypertrophic, restricted, and dilated;
3. Infectious and inflammatory processes (viral myocarditis, infective endocarditis);
4. Pulmonary hypertension resulting in right ventricular failure;
5. Toxic drugs.
The basic concept of cardiogenic shock is pump failure, not a surprise
to anyone, but again, impaired forward flow is the key. When cardiac
output decreases, the body responds with compensatory mechanisms.
Catecholamines (norepinephrine and epinephrine), parasympathetic
nervous stimulation, conduction disturbances, and dysrhythmias can all
affect heart rate, but typically tachycardia is seen. Systemic vascular
resistance (SVR) increases to “tighten” the arterial vascular circuit in an
attempt to maintain blood pressure. But these are only temporizing
measures. When caring for these patients, it helps to remember that
cardiac output = stroke volume x heart rate. So unless immediate
intervention is needed for a symptomatic rapid or relatively slow heart
rate, efforts are aimed at increasing the stroke volume. Understanding the
components of stroke volume helps direct patient management.
•
Components of stroke volume: Preload, afterload, and contractility
Preload is the amount of volume in the ventricle at end-diastolic filling.6 It is measured directly
during heart catheterization via the LVEDP or indirectly measured by utilizing the PCWP. Think of
preload as the end-diastolic “stretch” of the muscle determined by the volume of blood in the
ventricle. Every heart has an optimal preload. Remember Starling’s Law: Increased stretch results in
a more forceful contraction and greater stroke volume up to a physiologic limit. In other words, the
muscle fiber can be stretched up to a point and result in a good contraction, but if overstretched,
the contraction actually weakens and stroke volume decreases.
Afterload is resistance to ventricular ejection. Increased afterload translates into increased
work for the myocardium. Afterload for either ventricle is affected by several factors, the most
important being vascular resistance.6 When the arterial vascular circuit constricts in an attempt to
maintain pressure, afterload increases. More oxygen and energy is required for the heart to pump
volume out against this increased resistance — contributing to further problems for an ischemic
ventricle. Afterload is clinically estimated for the right ventricle by calculating the pulmonary
vascular resistance (PVR) and for the left ventricle, the systemic vascular resistance (SVR).
Finally, there’s contractility. Contractility is the velocity of myocardial fiber shortening at the
cellular level regardless of preload and afterload.6 It’s difficult to measure at the bedside, but one
would hope to see evidence of increased contractility when adding an inotropic agent such as
dopamine or dobutamine.
When thinking about the hemodynamics of cardiogenic shock, keep it simple:
The components of cardiac output are: Contractility, Rate, Afterload, and Preload, or “CRAP.” To
manage these patients, you’ve got to know CRAP! (This acronym has long been passed down to
many a critical care and cath lab staff and is helpful when managing cardiogenic shock). Every
therapeutic intervention is aimed towards improving or altering a component of cardiac output —
or something in CRAP.
• The spiral of cardiogenic shock
The underlying pathology of cardiogenic
shock is profound depression of contractility
resulting in a spiral of reduced CO, hypotension,
further coronary insufficiency, and further
reduction in contractility. Compensatory
mechanisms of tachycardia and increased SVR are
typically noted. However, a systemic
inflammatory response (fever, elevated white
count, low SVR) may also be seen.3
• Patient Presentation
In addition to tachycardia, patients often present with a
narrow pulse pressure (PP). Pulse pressure is the difference
between systolic and diastolic blood pressure and reflects
stroke volume. Decreased stroke volume causes the pulse
pressure to narrow (as is seen in cardiac tamponade). Signs
and symptoms of hypotension are present: Weak or absent
peripheral pulses; mottled extremities from low flow
states; diaphoresis; and pallor. Patients may be restless
with changes in level of consciousness. Remember that the
kidneys are “seeing” a low flow state when not receiving
adequate blood flow — with a response of retaining
volume and concentrating urine output.
• If left ventricular failure is present, pulmonary edema and dyspnea
are hallmarks of cardiogenic shock. An extra heart sound, S-3 or a
ventricular gallop, is an early sign of LV failure.5 A murmur may be
appreciated as the ventricle dilates from volume overload, resulting
in regurgitant flow. Murmurs may also occur with papillary muscle
dysfunction from ischemia. Chest pain, which can be typical or
atypical, might be present if the cause of failure is ischemic disease.
If right ventricular failure is the culprit, the patient will present
without pulmonary edema — clear lungs and a normal to slightly
raised PCWP. Persistent hypotension, elevated RA (CVP) pressure,
and jugular vein distention are often noted as volume “backs up”
from the right ventricle and forward flow declines. Suspect a right
ventricular infarction in patients exhibiting these symptoms who
present with an inferior wall MI. The reduction of preload
(hypovolemia, diuretic use, nitroglycerin) intensifies hypotension in
these individuals.5 Recording right-sided precordial leads and
utilizing echocardiography assists in the diagnosis.
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CRAP — Optimizing Preload
Does the patient have too much or too little preload? Higher filling pressures
may actually be necessary in some patients, but typically those in cardiogenic
shock have too much preload in the ventricle. The higher the PCWP (preload) and
the lower the cardiac index, the higher the mortality.4 If too much volume is
present for the heart to handle, there are the three well-recognized “P”s for
dealing with excessive preload: Pee the excess volume, park the excess volume, or
pump it on forward!
1. Patients have pulmonary edema and high PCWP? Diurese them — but avoid
hypovolemia (may worsen blood pressure—especially with a RV MI).
2. Poor contractility and decreased forward flow? Pump it forward with
inotropic support!
3. “Pull” extra volume off the heart (decrease venous return)—i.e.,
nitroglycerin to dilate venous beds. Park the volume if blood pressure tolerates.
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Intravenous diuretics such as furosemide and bumetanide not only cause diuresis
but also have an acute effect to increase venous capacity and decrease venous
return to the heart. Morphine, in addition to decreasing pain and anxiety, also
increases venous pooling.5 Even before there’s urine in the Foley bag (if you’re
lucky enough to see any urine in cardiogenic shock), these drugs have already
parked some excess volume. Now, pumping it forward usually means some
inotropic help with dopamine, dobutamine, inamrinone, or milrinone (Inocor® and
Primacor®, Sanofi-Synthelab Inc., New York, NY).
• CRAP — Optimizing Contractility
Inotropic support with a sympathomimetic
agent is indicated. With low blood pressure less
than 70 mmHg, norepinepherine 2 to 10 mg
/kg/min would be considered.5 Norepinepherine
is an alpha and beta-1 agonist, meaning it causes
vasoconstriction and increases contractility and
heart rate. Clinically, the alpha or vasoconstrictive
properties (increases SVR) are greater than beta1 effects, so its use should be limited for
temporary stabilization if possible.4
• Dopamine is a first-line inotropic agent in cardiogenic shock. It is
usually initiated at 3-5 mg/kg/min and titrated up to 10
mcg/kg/min. At higher doses, dopamine provides vasopressor
support. Doses greater than 10 mcg/kg/min may have undesirable
effects such as tachycardia and increased pulmonary shunting along
with the potential to decrease splanchnic perfusion and increase
pulmonary arterial wedge pressure.1 Another inotropic agent,
dobutamine, is a sympathomimetic amine with stronger beta
effects than alpha effect, producing vasodilation (decreasing SVR)
and increasing contractility. Dobutamine is initiated usually at 2.5–
5mg /kg/min and titrated up to 10 mg/kg/min.4 As it decreases
SVR, it may also decrease blood pressure making it difficult to use in
those with systolic pressures below 90 mmHg.5
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Working via a different mechanism than dopamine and dobutamine are the
phosphodiesterase inhibitors milrinone and inamrinone (formerly amrinone).
These drugs have both inotropic and vasodilating effects, thus increasing stroke
volume with both their contractile and afterload–reducing properties. These
vasodilator effects may cause hypotensive episodes to develop and careful
titration is needed. A loading dose may be given for both inamrinone and
milrinone. The loading dose for inamrinone (Inocor®) is 0.75 mg/kg followed by an
infusion of 5 to 10 mg/kg/min with total doses not to exceed 10 mg/kg/day.1
Milrinone (Primacor®) is approximately 15–20 times more potent than
inamrinone. In addition, clinical studies have reported significantly less
thrombocytopenia with milrinone as compared to inamrinone. Loading dose for
milrinone is 50 mg/kg followed by a maintenance dose of 0.375-0.750 mg
/kg/min.6 Careful dosing consideration of these drugs is required with hepatic and
renal dysfunction.
By increasing contractility, all inotropic agents increase myocardial workload
and in addition, may cause tachyarrhythmias, exacerbating myocardial ischemia.
• CRAP — Optimizing Heart Rate
With cardiogenic shock, bradycardia is usually not the problem,
but if present, a pacing wire may be necessary to sustain an
adequate rate and output. Tachycardia is typically present and is
related to sympathetic stimulation, a compensatory mechanism or
may result from inotropic drug support. Increased heart rates not
only decrease diastolic filling time, but also decrease coronary
artery perfusion time. In addition myocardial workload is increased.
Clearly, if the patient is in a lethal tachycardia or rapid
supraventricular tachycardia (SVT), the rhythm will need
termination.
It is important to try to maintain the atrial contribution to
stroke volume. Asynchrony between the atria and ventricles or the
absence of atrial contraction (development of atrial fibrillation) may
significantly reduce cardiac output.
• CRAP — Optimizing Afterload
It’s important to facilitate stroke volume
ejection and forward flow by reducing the SVR if
blood pressure permits. Some inotropic agents
reduce SVR. Vasodilators such as nitroglycerin
and sodium nitroprusside may also help.
Intravenous nitroglycerin is a coronary
vasodilator, but also tends to be at normal doses,
a venodilator predominately dilating the venous
bed. Nitroglycerin helps “park” volume.
Nitroprusside, on the other hand, is a more
balanced venous arterial vasodilator.6
• It is often a challenge to add these drugs because of low blood pressure.
As a result, these agents must be used cautiously, if at all, for besides
hypotension, a reflex tachycardia may occur and coronary perfusion
pressure can drop significantly. Vasodilator therapy should not be
attempted in patients with systolic pressure below 90 mmHg.6 So use
caution when reducing afterload in the presence of ischemic disease.
Afterload reduction is also the mainstay of stabilization for acute
mitral regurgitation (MR). In acute MR, blood flow is diverted back
through the mitral valve. There is less resistance to flow into the lower
pressure left atrium, verses forward flow out the aortic valve against
arterial resistance (SVR). Forward flow out the “front door” (aortic valve)
needs to be “encouraged”; therefore, therapies are targeted to reducing
the SVR. The optimal mechanical afterload reducer is the intraaortic
balloon pump, where a balloon is placed in the aorta distal to the
subclavian artery and counterpulsates the heart.
• With the normal arterial waveform, the dicrotic notch
signifies closure of the aortic valve closure and the
beginning of diastole. Inflation of the balloon at this
time augments diastolic pressure. This in turn increases
coronary perfusion pressure. When the balloon
deflates, aortic end-diastolic pressure decreases,
making it easier for the next stroke volume to be
ejected by the left ventricle. The IABP is effective for
the initial stabilization of patients with cardiogenic
shock. However, an IABP is not definitive therapy;
definitive diagnostic and therapeutic interventions
(surgical repair of the valve or revascularization) need
to be performed.
References Cardiogenic Shock
• 1. Sharma S, Zevitz ME. (2003). Cardiogenic shock.
www.Emedicine.com/MED/topic285.htm. [Electronic], retrieved 10/12/03.
2. Hostetler MA. (2002). Cardiogenic shock.
www.Emedicine.com/EMERG/topic530.htm. [Electronic], retrieved
10/12/03.
3. Hochman J. Cardiogenic Shock Complicating Acute Myocardial
Infarction: Expanding the Paradigm. Circulation 2003;107(24):2998-3002.
4. Lee J, Lee PC. Cardiology at a glance. New York City: McGraw-Hill, 2002.
5. Braunwald E. Recognition and management of patients with acute
myocardial infarction. In Goldman L, Braunwald E (eds). Primary
Cardiology. Philadelphia: WB Saunders, 1998.
6. Darovic GO. Hemodynamic Monitoring: Invasive and non-invasive
clinical application. Philadelphia: WB Saunders, 2002.
7. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern
Med 1999;131(1):47-59.
8. Pfisterer M. Right ventricular involvement in myocardial infarction and
cardiogenic shock. Lancet 2003;362(9381):392-394.
EVIDENCE-BASED PRACTICE (EBP)
GUIDELINE
• Use of Trendelenburg Position during
Hypotensive Episodes
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Nursing Research Council of United Hospital – 3/06
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HISTORY AND CLINICAL PRACTICE
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In the middle of the nineteenth century it was recognized that by raising the hips of a supine patient the
bulk of abdominal viscera would slide downward toward the diaphragm thereby providing a less cluttered
operative field for procedures involving the lower abdomen and pelvis. Friedrich Trendelenburg, a
pioneering German surgeon, adopted and popularized this practice in his surgical text of 1873. Then in
the early twentieth century, other physicians began advocating the use of Trendelenburg position in the
treatment of hemorrhagic shock because of its ability to divert blood from the lower extremities to the
central circulation, augmenting cardiac filling by increasing right and left ventricular preloads, stroke
volume and cardiac output. Despite leading physicians later questioning the efficacy of this position in
the 1950s, Trendelenburg continued as a mainstay of resuscitation in a wide variety of populations.1
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REVIEW OF EVIDENCE
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Several studies have measured the effects of Trendelenburg on hemodynamic parameters. These studies
have been conducted with healthy and acute/critical care populations using both observational and
experimental methods. Specific dependent variables measured include: Heart rate, blood pressure (BP),
cardiac output/cardiac index (CO/CI), central venous pressure (CVP), pulmonary artery wedge pressure
(PAWP), right and left atrial pressures (RA/LA), right and left end-systolic and end-diastolic ventricular
index (RVESVI/LVESVI), circulation time, carotid blood flow, internal jugular vein velocity, segmental
arm & leg blood flow, intrathoracic blood volume, and total blood volume displacement. Limitations of
these studies are the small sample sizes (N=10-76), lack of homogeneity of populations studied, as well as
variations in the angle (10-30o, and modified Trendelenburg with passive leg raising ranging from 45o to
60o) and duration (range 1-30 minutes) of the position.
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Fifteen studies from the medical and nursing literature were reviewed from 1964 to 2003. Three studies 24 (20%) demonstrated a statistically significant increase in BP and CO/CI in both healthy and critically ill
populations (N=10-22). In one study, 3 these changes disappeared after 10 minutes. The other 13 studies
(80%) did not find that Trendelenburg significantly increased either BP or CO/CI in a variety of samples
(animal model, healthy individuals, surgical and critically ill patients).5-17 Sample sizes of these studies
were also small, ranging from 8-76. Four of these studies showed a slight increase (~8-10%) in CO/CI in
a small percentage of patients (7-16 %).7-8,12-13 However, these significant changes appeared to be
transient and lasted for only 1-7 minutes after the change in position. It is unlikely these changes have
clinically significant effects on patients with hypotension or low CO.
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The majority of studies on the effects of Trendelenburg position do not lend support that this intervention
significantly increases either arterial BP or CO/CI. The level of evidence for this intervention is thought
to represent “Class III” evidence, indicating that Trendelenburg position is not useful in improving BP or
CO/CI in the hypotensive patient.
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In addition, expert opinion exists with regard to the possible harmful
effects associated with this intervention. In a review of physiological changes associated with this
position, Martin 1 delineates that the sequence of symptoms* that typically occur after placing a patient in
Trendelenburg position include:
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Anxiety & restlessness
Onset of pounding vascular headache
Nasal congestion that may force mouth breathing
Progressive dyspnea
Loss of cooperation (may include overt hostility)
Struggling efforts to sit upright
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* Hypotensive and mentally obtunded patients may first become transiently more alert and then
subsequently
lose the will to struggle
The presence of cardiovascular, pulmonary and central nervous system disease can make the position
harmful by increasing myocardial oxygen consumption and dysrhythmias; reducing respiratory expansion
and promoting hypoventilation and atelectasis, as well as altering ventilation/perfusion ratios from
gravitation of blood to poorly ventilated apex; and increasing venous congestion within and outside the
cranium leading to increased intracranial pressure. As a result, the Trendelenburg position may have
detrimental effects in patients with coronary artery disease and ischemia of the lower limbs, decreased
vital capacity such as in the obese, and increased intraocular and intracranial pressure and cerebral
edema.18 Because many of the studies reviewed assessed the effects of 200 or less, the presumption is
tenable that steeper angulation could produce greater physiological abnormalities. Similarly, the longer
the head down tilt is continued, it is likely the more pronounced the abnormalities might be.
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A. The evidence supporting the hemodynamic effects of Trendelenburg in treating shock is small and
does not reveal significant, beneficial or sustained changes in BP or CO/CI. Overall, the general
conclusion from all the evidence is that Trendelenburg is probably not a useful position in
resuscitative situations to improve BP or CO/CI. Since Trendelenburg may also be associated with
harmful effects to the respiratory, neurological and vascular systems (especially in the presence of
pathology) this position should be used with caution.
B. The available evidence on Trendelenburg position lacks strength due to limitations in scientific rigor.
High-quality clinical studies of the risks and benefits of Trendelenburg position in hypotensive
patients are warranted. Trials that investigate optimal positions for resuscitation are also needed.18
References: EBP Trendelenberg
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1. Martin J. (1995). The Trendelenburg position: A review of current slants about head down tilt. J
Amer Assoc Nurs Anesths. 63 (1): 29-36.
2. Pricolo V, Burchard K, Singh A, Moran J, & Gann D. (1986). Trendelenburg versus PASG
application: Hemodynamic response in man. J Trauma. 26 (8): 718-726.
3. Gentili D, Benjamin E, Berger S, & Iberti T. (1988). Cardiopulmonary effects of the head-down
tilt position in elderly postoperative patients: A prospective study. Southern Medical J. 81 (10):
1258-1260.
4. Terai C, Anada H, Matsushima S, Shimizu S, & Okada (1995). Effects of mild Trendelenburg on
central hemodynamics and internal jugular vein velocity, cross-sectional area, and flow.
American J Emerg Med. 13 (3): 255-258.
5. Guntheroth W. (1964). The effect of Trendelenburg’s position on blood pressure and carotid
flow. Surgery, Gyn & Obstet pp. 345-348.
6. Taylor J, & Weil M. (1967). Failure of the Trendelenburg position to improve circulation during
clinical shock. Surgery, Gyn & Obstet , pp. 1005-1010.
7. Sibbald W, Paterson N, Holliday R, & Baskerville J. (1979). The Trendelenburg position:
Hemodynamic effects in hypotensive and normotensive patients. Critical Care Med. 7 (5): 218224.
8. Gaffney F, Bastian B, Thal E, Atkins J, & Blomquist C. (1982). Passive leg raising does not
produce a significant or sustained Autotransfusion effect. J Trauma. 22 (3): 190-193.
9. Sing R, O’Hara D, Sawyer M, & Marino P. (1994). Trendelenburg position and oxygen
transport in hypovolemic adults. Annals Emerg Med. 23 (3): 564-567.
10. Bivins H, Knopp R, dos Santos. (1985). Blood volume distribution in the Trendelenburg
position. Annals Emerg Med. 14 (7): 641-643.
11. Haennel R, Teo K, Snydmiller G, Qinnery J, & Kappagoda C. (1988). Short-term cardiovascular
adaptations to vertical head-down suspension. Arch Physical Med Rehab. 69: 352-357.
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12. Wong D, Tremper K, Zaccari J, Hajduczek J, Konchiegeri J, & Hufstedler S. (1988). Acute
cardiovascular response to passive leg raising. Critical Care Med 16 (2): 123-125.
13. Reich D, Konstadt S, Raissi S, Hubbard M, & Thys D. (1989). Trendelenburg position and
passive leg raising do not significantly improve cardiopulmonary performance in the anesthetized
patient with coronary artery disease. Critical Care Med. 17 (4): 313-317.
14. McHugh G, Robinson B, & Galletly D. (1994). Leg elevation compared with Trendelenburg
position: Effects on autonomic cardiac control. British J Anaesthesia. 73: 836-837.
15. Ostrow L, Hupp E, & Topjian D. (1994). The effect of Trendelenburg and modified Trendelenburg
positions on cardiac output, blood pressure and oxygenation: A preliminary study. Amer J Critical
Care. 3 (5): 382-386.
16. Boulain T, Achard J, Teboul J, Richard C, Perrotin D, & Ginies G. (2002). Changes in BP
induced by passive leg raising predict response to fluid loading in critically ill patients. Chest.
121 (4): 1245-1252.
17. Reuter D, Felbinger T, Schmidt C, Moerstedt K, Kilger E, Lamm P et al. (2003). Trendelenburg
positioning after cardiac surgery: Effects of intrathoracic blood volume index and cardiac
performance. European J Anaesth. 20: 17-20.
18. Bridges N, Jarquin-Valdivia A. (2005). Use of the Trendelenburg position as the resuscitation
position : To T or not to T ? Amer J Critical Care. 14 (5): 364-368.
LEVELS OF
EVIDENCE
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Class I
Definitely recommended
Supported by excellent evidence,
with at least 1 prospective
randomized, controlled trial.
Class I interventions are always
acceptable, safe & effective.
Considered definitive standard of care
Class IIa
Acceptable & useful
Supported by good to very good
evidence. Weight of evidence and
expert opinion strongly in favor.
Class IIa interventions are acceptable,
safe & useful. Considered intervention
of choice by majority of experts.
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Class IIb
Acceptable & useful
Supported by fair to good
evidence. Weight of evidence and
expert opinion not strongly in
favor.
Class IIb interventions are also
acceptable, safe and useful. Considered
optional or alternative interventions by
majority of experts.
Indeterminate
Promising, evidence
lacking, immature
Preliminary research stage.
Evidence: No harm but no
benefit. Evidence insufficient to
support a final class decision.
Indeterminate: Describes treatments
of promise but limited evidence.
Class III
May be harmful;
no benefit documented
Not acceptable, not useful, may be
harmful.
Class III refers to interventions with no
evidence of any benefit; often some
evidence of harm