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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)

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Module 15 shock

Module 15- Shock!

John Nation, RN, MSN

From the notes of Nancy Jenkins, RN, MSN


Shock

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 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

Types of Shock-

Low blood flow-

  • Cardiogenic shock

  • Hypovolemic shock

    Maldistribution of blood flow-

  • Neurogenic shock

  • Anaphylactic shock

  • Septic shock


Etiology and pathophysiology

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

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 d1

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 d2

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 d3

Cardiogenic Shock (Cont’d)

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


Cardiogenic shock cont d4

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 d5

Cardiogenic Shock (Cont’d)

Treatment (Cont’d)

  • Medications (depends on cause):

    • Aspirin

    • heparin

    • Dopamine

    • Norepiniphrine

    • dobutamine

    • Diuretics

    • Vasodilators

    • Amiodarone


Pawp monitoring

PAWP Monitoring


Module 15 shock

IABP


Cardiogenic shock cont d6

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

Hypovolemic Shock-

  • Loss of intravascular fluid volume

  • Volume inadequate to fill the vascular space

  • Categorized as absolute or relative hypovolemia


Hypvolemic shock cont d

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

Hypovolemic Shock (Cont’d)

Causes:

  • Bleeding

  • Vomiting

  • Diarrhea

  • Diabetes insipidus

  • Diuresis

  • Third spacing


Hypovolemic shock cont d1

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 shock1

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 d2

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 d3

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 shock2

Hypovolemic Shock

  • What is often the priority in the treatment of hypovolemic shock?

  • How might you recognize the development of hypovolemic shock?

  • What would you do about it?


Neurogenic shock

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

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 d1

Neurogenic Shock (Cont’d)

Clinical Manifestations (Cont’d)

  • Bladder dysfunction

  • Paralysis below level of lesion

  • Bowel dysfunction


Neurogenic shock cont d2

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

Neurogenic (Cont’d)

Late Signs-

  • Skin pale and cool


Neurogenic shock cont d3

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

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

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 d1

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 d2

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


Module 15 shock

  • From Seton. Educational use only.


Anaphylactic shock1

Anaphylactic Shock

  • What are you worried about with a medication reaction?

  • What are you watching for?


Septic shock

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

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 shock1

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 d1

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 d2

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


Module 15 shock

  • From Seton. Educational use only.


Obstructive shock

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

Common Diagnostic Tests

  • CBC

  • BMP

  • Arterial blood gases

  • Blood cultures

  • Cardiac enzymes (cardiogenic shock)

  • Glucose


Common diagnostic tests cont d

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

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

Common Nursing Diagnoses

  • Decreased cardiac output

  • Altered tissue perfusion

  • Fluid volume deficit

  • Anxiety

  • Fear


Module 15 shock

LVAD implantation (23 minutes into clip)


Stages of shock

Stages of Shock

Compensatory 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

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

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

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

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

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

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

Interventions

Assessment (Respiratory)-

  • Respiratory rate and effort

  • Pulse oximetry

  • ABGs for acid/base balance

  • Intubation/ ventilation


Module 15 shock

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


Module 15 shock

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)

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

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


Module 15 shock

  • 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

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 care1

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

The End!


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