Shock! - Austin Community College
Download
Report
Transcript Shock! - Austin Community College
Module 15A- Shock!
John Nation, RN, MSN
From the notes of Nancy Jenkins,
RN, MSN
ShockSummary–
–
–
–
–
–
Lewis p. 1772-1798, 1738-1746
Types of Shock
Stages of Shock
Management of Shock
Nursing Interventions
Systemic Inflammatory Response Syndrome
(SIRS)
– Multiple Organ Dysfunction Syndrome (MODS)
Shock Defined
Shock- Clinical syndrome characterized
by decreased tissue perfusion and
impaired cellular metabolism resulting in
an imbalance between the supply and
demand for oxygen and nutrients
– Put simply, not enough oxygen and not
enough nutrients for body
Types of ShockLow blood flow• Cardiogenic shock
• Hypovolemic shock
Maldistribution of blood flow• Neurogenic shock
• Anaphylactic shock
• Septic shock
Etiology and Pathophysiology
Cardiogenic shock– Occurs when systolic or diastolic dysfunction of
the pumping of the heart causes decreased
cardiac output
– Cardiac output= stroke volume x heart rate
– Causes include myocardial infarction,
cardiomyopathy, blunt cardiac injury (trauma),
severe systemic or pulmonary hypertension,
cardiac tamponade, arrhythmias, valvular
defects,and myocardial depression from metabolic
problems.
Cardiogenic Shock
Cardiogenic Shock (Cont’d)
Clinical Manifestations:
–
–
–
–
–
–
–
–
–
Tachycardia
Hypotension
Narrowed pulse pressure
Tachypnea
Pulmonary congestion
Cyanosis
Cool, clammy skin
Confusion/ agitation
Decreased capillary refill time
Cardiogenic Shock (Cont’d)
Treatment– Restore blood flow to myocardium- early PCI!
– Thromboyltic therapy, angioplasty, stenting,
emergency revasularization, valve replacement
– Hemodynamic monitoring PAWP
– Intraaortic balloon pump (IABP) 50. IABP
– Ventricular assist device VAD video
– Transplant (rarely)
Cardiogenic Shock (Cont’d)
Treatment (Cont’d)
– Medications: aspirin, heparin, dopamine,
norepiniphrine, diuretics, vasodilators
PAWP Monitoring
IABP
Cardiogenic Shock (Cont’d)
• Mortaliaty rate of 80-90% when caused
by acute MI
• Prior MI, increasing age, and oliguria
are associated with worsening
outcomes
Hypovolemic Shock• Loss of intravascular fluid volume
• Volume inadequate to fill the vascular
space
• Categorized as absolute or relative
hypovolemia
Hypvolemic Shock (Cont’d)
Absolute hypovolemia– Results from fluid loss via hemorrhage,
gastrointesinal (GI) loss (vomiting,
diarrhea), fistula drainage, diabetes
insipidus, hyperglycemia, or diuresis
Relative hypovolemia– Results from fluid moving out of the
vascular space and into the extravascular
space- aka third spacing
Hypovolemic Shock
Hypovolemic Shock (Cont’d)
Clinical Manifestations– Depend on extent of injury, age, general health
status
– Decrease in venous return, preload, stroke
volume, and cardiac output
– Increase in heart rate, increase in respiratory rate
– Decrease in stroke volume, pulmonary artery
wedge pressure, and urine output
Hypovolemic Shock (Cont’d)
Treatment– Stop source of fluid loss
– Restore circulating volume
– 3:1 rule- 3 ml of isotonic crystalloid for
every 1 ml of estimated blood loss
Neurogenic Shock– Hemodynamic phenomenon occuring after
spinal injury at T5 or above
– Usually within 30 minutes of injury, can last
up to 6 weeks
– Causes massive vasodilation without
compensation secondary to the loss of
sympathetic nervous system
vasoconstrictor tone
– Can also be caused by spinal anesthesia
Neurogenic Shock
Neurogenic Shock (Cont’d)
Clinical manifestations– Bradycardia (from unopposed
parasympathetic stimulation)
– Hypotension (from massive vasodilation)
– Hypothermia (due to heat loss)
Neurogenic Shock (Cont’d)
Early Signs– Blood pools in venous and capillary beds
– Skin warm and pink
– Pulse slow and bounding
– Decreased BP
– Decreased temperature
– Decreased MAP
Neurogenic (Cont’d)
Late Signs– Skin pale and cool
Neurogenic Shock (Cont’d)
Treatment– Depends on the cause
– If spinal cord injury, promote spinal stability
– Vasopressors and atropine for hypotension
and bradycardia (respectively)
– Fluids administered cautiously
– Monitor for hypothermia
Anaphylactic Shock
– Acute and life-threatening allergic reaction
(hypersensitivity) reaction
– Can be caused by drugs, chemicals, vaccines,
food insect venom
– Causes massive vasodilation, release of
vasoactive mediators, and an increase in capillary
permeability
– Fluid shift from the vascular space to the interstitial
space
– Respiratory distress secondary to laryngeal
edema, severe bronchospasm, or circulatory
failure from vasodilation
Anaphylactic Shock (Cont’d)
Clinical Manifestations–
–
–
–
–
–
–
–
Anxiety, confusion
Dizziness
Chest pain
Incontinence
Swelling of lip and tongue
Wheezing, stridor
Flushing, pruritus, and uticaria
angioedema
Anaphylactic Shock (Cont’d)
Treatment– Epinephrine is the drug of choice
– Diphenhydramine used to block massive release
of histamine
– Maintain patent airway
– Nebulized bronchodilators (albuterol)
– Intubation or cricothyroidotomy may be needed
– Fluid replacement, primarily with colloids
– corticosteroids
Septic Shock
Septic shock- Presence of sepsis with
hypotension, despite fluid resuscitation,
with decreased tissue perfusion
Sepsis- systemic inflammatory response to
an infection
• Over 750,000 clients diagnosed with sever
sepsis annually and 28% to 50% die
Septic Shock
Septic Shock (Cont’d)
Course– Septicemia (initially bacteremia) causes
inflammatory cascade
– Commonly caused by gram negative
bacteria
– If gram positive infection (Staphylococcus
and streptococcus), up to 50% mortality
rate
Septic Shock (Cont’d)
Clinical Manifestations– Increased or decreased temperature
– Biventricular dilations causing decreased ejection
fraction
– Hyperventilation, respiratory alkalosis, respiratory
acidosis, crackles, ARDS
– Decreased urine output
– Skin warm and flushed, then cool and clammy
– Altered LOC
– Paralytic ileus, GI bleeding
– & WBC, platelets, lactate, glucose,
urine specific gravity, urine Na, positive blood
cultures
Septic Shock (Cont’d)
Treatment–
–
–
–
–
–
–
Large amounts of fluid replacement
Vasopressor drug therapy
Corticosteroids
Antibiotics
Drotrecogin alpha (Xigris)
Glucose less than 150
Stress ulcer prophylaxis with H2- receptor
blockers and DVT prophylaxis
Diagnostic Tests
•
•
•
•
•
•
RBC, hemoglobin, hematocrit
Arterial blood gases
Blood cultures
Cardiac enzymes (cardiogenic shock)
Glucose
DIC (Disseminated Intravascular
Coagulation) screen: FSP, fibrogen level,
platelet count, PTT and PT/INR, and D-dimer
• Lactic Acid
• Liver enzymes- ALT, AST, GGT
Diagnostic Tests (Cont’d)
Electrolytes– Sodium level increased early, decreased
later if hypotonic fluid administered) (
– Potassium decreased, then increased later
with celluar breakdown and renal failure
Common Nursing Diagnoses
•
•
•
•
•
Decreased cardiac output
Altered tissue perfusion
Fluid volume deficit
Anxiety
Fear
LVAD implantation (23 minutes into clip)
A pt. with severe trauma has been treated for hypovolemic shock.
The nurse recognizes that the patient is in the refractory stage of
show when assessment findings include:
1.
Blood Pressure of
98/64
2. Responsive to
painful stimuli only
3. Profound
hypotension
unresponsive to IVF
or vasopressors
4. Jaudice
A patient in shock has a nursing diagnosis of fear related to severity
of condition and perceived threat of death. The most appropriate
initial intervention is to:
1. Administer
antianxiety agent
2. Call a member of the
clergy to visit the
patient
3. Allow family
members to visit as
much as possible
4. Inform the patient of
the current POC and
its rationale
When administering any vasoactive drug during the treatment of
shock, the nurse knows that the goal of this therapy is to:
1. Increase urine
output
2. Maintain a MAP of at
least 60 mm Hg
3. Dilate vessels to
improve tissue
perfusion
4. Constrict vessels to
maintain BP
Stages of Shock
Compensatory Shock Mean Arterial Pressure (MAP)
blood pressure
cardiac output
Sympathetic nervous system (SNS) stimulation
causes vasoconstriction. Blood flow to heart and
brain maintained, while blood flow to the kidneys,
GI tract, skin, and lungs is diverted
– Decreased blood flow to kidneys causes activation
of renin-angiotensin system, leading to sodium
retention and postassium extretion
– In this stage the body is able to compensate for
changes in tissue perfusion
–
–
–
–
Compensatory Stage of Shock
Progressive Shock
• Altered capillary permeability (3rd spacing)
• Alveolar and pulmonary edema, ARDS, PA
pressures
• cardiac output, coronary perfusion, can
cause arrhythmias and MI
• Acute tubular necrosis
• Jaundice, ALT,AST GGT
• DIC
• Cold, clammy skin
Progressive Stage of Shock
Refractory Stage
• Anaerobic metabolism- lactic acid build-up
• Increased capillary blood leak
• Profound hypotension, inadequate to perfuse
vital organs
• Respiratory failure
• Anuria
• DIC
• hypothermia
Refractory Stage of Shock
Collaborative Care
Successful management involves:
– Identifying at risk clients
– Integration of client’s medical history,
assessment findings to establish diagnosis
– Interventions to address cause of
decreased perfusion
– Protection of organs
– Multisystem supportive care
Collaborative Management
(Cont’d)
– Start with ABCs! Ensure patent airway and
oxygen delivery
– Volume expansion and fluid administration
cornerstone of treatment of septic,
hypovolemic, and anaphylactic shock
– Primary goal of therapy is correction of
decreased tissue perfusion
– Hemodynamic monitoring, drug therapy,
ciculatory assist
Nursing Implementation
Health Promotion– Identify at risk clients
– Prevent shock (monitoring fluid balance,
good hand washing to prevent infection,
community education and health
promotion)
Interventions (Acute)
• Assess neurologic status- check LOC every
hour or more often
• Monitor heart rate/ rhythm, BP, central venous
pressure, pulmonary artery pressure, cardiac
output
• Trendelenburg position not supported by
research and may compromise pulmonary
function and increase ICP
• Monitor EKG for dysrhythmias, S3 or S4 heart
sounds
Interventions
Assessment (Respiratory)– Respiratory rate and effort
– Pulse oximetry
– ABGs for acid/base balance
– Intubation/ ventilation
Assessment– Hourly urine output
– If less than 0.5 ml/kg/hour, may indicate
inadequate kidney perfusion
– BUN and creatinine
– Temperature
– Capillary refill
– Monitor skin for pallor, flushing, cyanosis,
diaphoresis, piloerection
Assessment (Cont’d)– Check bowel sounds
– If NG tube present, check drainage for
blood
– Passive ROM and oral care
– Talk with client, even if sedated or
intubated
Systemic Inflammatory
Response Sydrome (SIRS)
Systemic Inflammatory Response
Syndrome (SIRS)- a systemic
inflammatory response to a variety of
insults, including infection, ischemia,
infarction, and injury
– Characterized by generalized inflammation
of organs
Multiple Organ Dysfunction
Syndrome (MODS)
– Results from SIRS
– Characterized by failure of two or more
organ systems such that homeostasis can
not be obtained without intervention
– Often culminates in ARDS
– Can cause massive vasodilation and
myocardial depression
– Commonly manifests as changes in LOC
– Acute renal failure common
• GI tract highly vulnerable to ischemic
injury secondary to shunting in early
stages
• At risk for ulceration and GI bleeding
• Potential for bacterial translocation from
GI tract to cirulation
• Causes hypermetabolic state
• Failure of coagulation system manifests
as DIC
• Electrolyte changes and fluid shifts
A patient with a gunshot wound to the abdomen is being treated for
hypovolemic and septic shock. To monitor the patient for early
organ damage associated with MODS, it is most important for the
nurse to assess:
1. Urine output
2. Lung sounds
3. Peripheral
circulation
4. Central venous
pressure
The development of MODS is confirmed
in a patient who manifests:
1.
2.
3.
4.
Urine output of 30 ml/hr, a
BUN of 65 mg/dl, and a WBC
of 1120/ul
Upper GI bleeding, GCS
score of 7, and a Hct of 25%
RR of 45/min, PaCO2 of 60,
and a chest x-ray with
bilateral patchy infiltrates
An elevated serum amylase
and lipase, serum creatinine
of 3.8 mg/dl, and a platelet
count of 15,000/ul
Management of SIRS and MODS
• Prognosis with MODS poor
• Vigilant assessment
• Prevent infection, maintain tissue
oxygenation, nutritional and metabolic
support, support individual failing
organs
A teenager arrives by private car. He is alert and ambulatory, but
his shirt and pants are covered with blood. He and his hysterical
friends are yelling and trying to explain that they were goofing
around and he got poked in the abdomen with a stick. Which of the
following comments should be given first consideration?
.
1.
2.
3.
4.
“There was a lot of blood. We
used 5 bandages.”
“Thankfully we finally got the
stick out just now”
“That stick had a lot of mud
on it!”
“He’s diabetic!”
Emergency and ambulatory care nurses are among the first health
care workers to encounter victims from a bioterrorist attack. What is
the highest priority for the ED staff in the event of a biochemical
incident?
1. Report event to
the CDC
2. Decontaminate
victims
3. Protect
themselves
4. Triage per
protocol
At 9pm, you admit a 63 year-old with a diagnosis of acute
myocardial infraction to the ED. The physician is considering the
use of fibrinolytic therapy with tissue plasminogen activator (tPA,
alteplase (Activase)). Which information is most important to
communicate to the physician?
1. Pt was treated with
TPA 8 months ago
2. Pt takes coumadin
for A-fib. The INR is
1.0 today
3. Pt has T-Wave
inversions on ECG
4. Chest pain has been
continuous since
1pm
Note:
Questions are from Prioritization,
Delegation, and Assignment (LaCharity,
Kumagai, and Bartz)
The End!