Module 15A- Shock!

John Nation, RN, MSN

From the notes of Nancy Jenkins, RN, MSN

Shock-

Summary-– 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 Shock-

Low 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 ShockCompensatory 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. Urine output of 30 ml/hr, a BUN of 65 mg/dl, and a WBC of 1120/ul

2. Upper GI bleeding, GCS score of 7, and a Hct of 25%

3. RR of 45/min, PaCO2 of 60, and a chest x-ray with bilateral patchy infiltrates

4. 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. “There was a lot of blood. We

used 5 bandages.”

2. “Thankfully we finally got the stick out just now”

3. “That stick had a lot of mud on it!”

4. “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!