Module 15- 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)– Critical Care

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

Cardiogenic Shock (cont’d)

• Causes include:• myocardial infarction• cardiomyopathy• blunt cardiac injury (trauma)• severe systemic or pulmonary hypertension• cardiac tamponade• arrhythmias• valvular defects• myocardial depression from metabolic problems.

Cardiogenic Shock (Cont’d)

Clinical Manifestations:– Tachycardia– Hypotension– Narrowed pulse pressure– Tachypnea– Increased SVR, CVP, and PAWP– Pulmonary congestion– Cyanosis– Cool, clammy skin– Confusion/ agitation– Decreased capillary refill time

Cardiogenic Shock (Cont’d)

Laboratory/ Diagnostic Studies:– Cardiac enzymes (troponin levels)– B-type natriuretic peptide (BNP)– ECG– Chest X-Ray– Echocardiogram– Heart Cathetarization (left, right or both)

Cardiogenic Shock (Cont’d)

• Initially, what clinical condition does this sound similar to?

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 (depends on cause):

• Aspirin

• heparin

• Dopamine

• Norepiniphrine

• dobutamine

• Diuretics

• Vasodilators

• Amiodarone

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 (Cont’d)

Causes:– Bleeding– Vomiting– Diarrhea– Diabetes insipidus– Diuresis– Third spacing

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

Hypovolemic Shock

Clinical Manifestations (Cont’d):– Decrease in stroke volume, pulmonary artery

wedge pressure, and central venous pressure

– Decrease in urine output, absent bowel sounds, cool, clammy skin

– Anxiety, confusion, agitation

Hypovolemic Shock (Cont’d)

Lab/ Diagnostic Tests:– Find the source of blood loss

• CT, ultrasound, surgery

– CBC, electrolytes, blood gases, lactate level

– SpO2– Hourly urine output monitoring

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

Hypovolemic Shock

1) What is often the priority in the treatment of hypovolemic shock?

2) How might you recognize the development of hypovolemic shock?

3) What would you do about it?

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 (Cont’d)

Clinical manifestations-– Bradycardia (from unopposed

parasympathetic stimulation)– Hypotension (from massive vasodilation)– Hypothermia (due to heat loss)

• Initially, skin may be warm due to vasodilation• Later, skin may be cool, depending on ambient

temperature

Neurogenic Shock (Cont’d)

Clinical Manifestations (Cont’d)– Bladder dysfunction– Paralysis below level of lesion– Bowel dysfunction

Neurogenic Shock (Cont’d)

Early Signs-– Blood pools in venous and capillary beds– Skin warm and pink– Pulse slow and bounding– Decreased BP– 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

Anaphylactic Shock (Cont’d)

– 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, shortness of breath – Flushing, pruritus, and uticaria (hives)– 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 (video) be needed– Fluid replacement, primarily with colloids– corticosteroids

• From Seton. Educational use only.

Anaphylactic Shock

• What are you worried about with a medication reaction?

• What are you watching for?

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 severe sepsis annually and 28% to 50% die

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

Patho:– Invading microorganisms result in massive

inflammatory response:• Causes endothelial damage, microemboli,

vasodilation, increased capillary permeability, platelet aggregation, myocardial depression

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) (no longer used)– Glucose less than 150– Stress ulcer prophylaxis with H2- receptor

blockers and DVT prophylaxis

• From Seton. Educational use only.

Obstructive Shock

• Physical obstruction to blood flow

• Causes:– Cardiac tamponade, tension

pneumothorax, PE, left ventricular thrombi

• Decreased cardiac output, increased afterload

• Fix the underlying problem is primary treatment

Common Diagnostic Tests

• CBC• BMP• Arterial blood gases• Blood cultures• Cardiac enzymes (cardiogenic shock)• Glucose

Common Diagnostic Tests (Cont’d)

• 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 in early shock, then increased later with cellular breakdown and renal failure

Common Nursing Diagnoses

• Decreased cardiac output

• Altered tissue perfusion

• Fluid volume deficit

• Anxiety

• Fear

LVAD implantation (23 minutes into clip)

Stages of ShockCompensatory Shock-

Mean Arterial Pressure (MAP) blood pressure (but adequate to perfuse vital organs) 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 potassium excretion

– In this stage the body is able to compensate for changes in tissue perfusion

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

Refractory Stage

• Anaerobic metabolism- lactic acid build-up• Increased capillary blood leak• Profound hypotension, inadequate to perfuse vital

organs• Respiratory failure• Unresponsive • Anuria• DIC• hypothermia

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, circulatory 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 Syndrome (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– Two or more of the following conditions:

temperature >38.5°C (101.3 F) or <35.0°C (95.0 F); heart rate of >90 beats/min; respiratory rate of >20 breaths/min or PaCO2 of <32 mm Hg; and WBC count of >12,000 cells/mL, <4000 cells/mL, or >10 percent immature (band) forms

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

Critical Care

• Care of the critically ill patient

• Invasive monitoring capabilities

• Bedside procedures possible

• 2 to 1 patient to nurse ratio

• Intensivists or pulmonary/ critical care physicians and advanced practice nurses

Critical Care

• Post-surgical pathways often include going to ICU

• Certain medications, devices, and frequency of testing require placement in ICU

• Medications must be reconciled with any move to or from critical care to other level of care

• Notify family members

The End!