Shock

Question 1

Anoxia

Answer 1

Total depletion/absence of oxygen

Question 2

Hypoxemia

Answer 2

Low oxygen in the blood

Question 3

Hypoxia

Answer 3

Abnormally low oxygen content in any tissue or organ

Question 4

What is shock?

Answer 4

• A state of inadequate tissue perfusion resulting in inadequate oxygen delivery to the cell
• Caused by many factors including anything that alters heart function, blood pressure, or blood volume

Question 5

What results when unable to to correct or reverse shock?

Answer 5

Inability to correct and reverse shock results in increasing oxygen debt/deficit, acidosis, organ system dysfunction and eventually death

Question 6

What are the keys to preventing shock?

Answer 6

Key to prevention is rapid recognition and intervention before a refractory or irreversible shock state occurs

Question 7

What happens at the cellular level in shock?

Answer 7

Inadequate tissue perfusion results in impaired cellular metabolism
This results in:
1. Impaired oxygen use
2. Impaired glucose use (i.e. impaired uptake which can be caused by impairment of Na/K pump)
3. Buildup of metabolic end products (such as lactic acid and nitrous oxide which can rapidly build up in high concentrations in the cell and blood thus lowering the pH and causing acidosis)

Question 8

What occurs with impaired oxygen use ?

Answer 8

• In shock states, without adequate oxygen, cells must use the less efficient anaerobic pathway
• This pathway generates an insufficient amount of ATP to maintain normal cellular metabolism
• Acidosis results
• With limited ATP, cells lose their ability to maintain an electrochemical gradient and the sodium-potassium pump fails

Question 9

What occurs with impaired glucose use?

Answer 9

• Due to impaired glucose delivery or from impaired glucose uptake by the cell
• Hormonal and neurochemical release during shock states also increase the amount of glucose available
  Cortisol: increases blood sugar through gluconeogenesis
  Growth hormone: anti-insulin activity
  Catecholamines: NE inhibits insulin
  Net result is a buildup of glucose in the extracellular environment resulting in hyperglycemia

Question 10

What occurs with a build-up of metabolic end products?

Answer 10

• Impaired cellular metabolism results in a buildup of metabolic end products (i.e. lactic acid) that are toxic to cells
• This buildup results in further disruption to cellular function and membrane integrity
• Lactic acidosis: Lactate levels >5 mmol/L and serum pH <7.35

Question 11

What are the systemic effects of shock on your lungs?

Answer 11

• Circulatory deprivation results in tissue hypoxia and anoxia
  Shock causes:
• Decreased gas exchange
• Tachypnea
• Pulmonary edema (ARDS: Acute respiratory distress syndrome)
• Respiratory failure is a major cause of death in shock
  ARDS is when the alveoli inflame, fills with liquid and collapses, gas exchange is unable to occur

Question 12

What are the systemic effects of shock on your heart?

Answer 12

Myocardial deterioration is one of the major causes of death in shock
Shock causes:
- Decreased cardiac output
- Hypotension
- Release of myocardial depressants (MDF - myocardial depressant factor) – causes significant reduction in cardiac output

Question 13

What are the systemic effect of shock in the blood?

Answer 13

Coagulation abnormalities

• During shock, hypoxia is caused by the slow-movement of blood in the capillaries; anaerobic metabolism begins and increases the production of lactic acid
• Slow-moving acidic blood is hypercoagulable
• When clotting factors are present along with the acidic blood of shock, widespread intravascular clotting may occur in the vessels (DIC)

Question 14

What is DIC?

Answer 14

DIC (Disseminated Intravascular Coagulation)

• Causes multiple thrombi or emboli in microvascular circulation
• Body attempts to break down clots, but this also includes normal clot formation (in response to traumatic bleeding)
• Treatment includes: treating the precipitating cause, anticoagulant therapy, replacement of clotting factors (blood transfusion)

Question 15

What are some lab tests used to diagnose DIC?

Answer 15

Lab findings: 
	Thrombocytopenia; 
	Prolonged PT, aPTT, thrombin time; 
	Decreased fibrinogen; 
	Elevated D-dimers 

• Thrombocytopenia indicates a low blood platelet count
• PT is a blood test that measures the amount of time it takes for your blood to clot (often prolonged)
• Thrombin time this is a screening coagulation test designed to test fibrin formation from fibrinogen and plasma (also prolonged)
• Fibrinogen or factor I is a glycoprotein that helps in the formation of blood clot and normally we see decreased fibrinogen
• D-dimer is fibrin degradation product – a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis and these levels are usually elevated

Question 16

What are some neuroendocrine manifestations and mechanisms in shock? (i.e. tachycardia in shock)

Answer 16

• Cool, pale skin, increased BP: SNS stimulation, NE release -> vasoconstriction
• Tachycardia: SNS stimulation, epinephrine release
• Hyperglycemia: SNS stimulation, epinephrine release, growth hormone release
• Altered immune response: the release of glucocorticoids -> increase in ACTH
• Water retention (weight gain): Increase in ADH & aldosterone leads to sodium and water retention
• Oliguria: Decreased tissue perfusion

Question 17

How does shock affect the immune system?

Answer 17

Depression of immune function; shock severely depresses macrophages

• Macrophages are located in the blood and tissues, shock reduces the capacity of macrophages to remove bacteria and toxins from the bloodstream
• Therefore people suffering shock are more susceptible to bacteria and endotoxins

Question 18

How does shock affect the renal system?

Answer 18

Decreased UO -> reflective of status of circulation through vital organs

• the rate of urinary production reflects visceral blood flow and body fluid imbalance

Question 19

How does shock affect the GI system?

Answer 19

Ileus, hypoxia -> tissue necrosis and sepsis; impaired liver function

• Under sympathetic stimulation, vagal stimulation to the GI tract slows or stops resulting in ileus with an absence of peristalsis
• A lack of nutrient blood supply to the intestines increases the risk of tissue necrosis and sepsis
• The liver is also at risk for impaired circulation, during shock – the liver has an impaired ability to detoxify and may also release vasoactive substances

Question 20

What three components does adequate circulating volume depend on?

Answer 20

• Heart
• Vascular tone
• Blood volume
• A minor impairment in one can be compensated by the other two
• If prolonged or severe impairments occur, this leads to shock

Question 21

How is blood circulation controlled and driven? Where is blood from the heart is delivered? Where is circulation slowest?

Answer 21

• Blood flows throughout body due to the driving pressure as it exits the left ventricle
• The size of the body’s larger vessels is controlled by the autonomic nervous system (ANS)
• Blood is delivered into arterioles where it can be stored and released more consistently into the capillaries
• Blood flows slowly through capillaries (greatest demand)

Question 22

What controls microcirculation?

Answer 22

• Microcirculation is controlled locally by vasoactive substances released in the area by the actions of various types of cells
• ## Blood flow through capillary bed is influenced by the needs of the cells near the vessels

Question 23

Arterial baroreceptor & chemoreceptor responses to changes in arterial pressure

Answer 23

• When there is blood loss, there is a decrease in arterial blood pressure
• The body can quickly detect a fall in blood pressure through its arteriole
• Cardiopulmonary baroreceptors and then activate the sympathetic adrenergic system to stimulate the heart increasing heart rate and contractility and constrict blood vessels thereby increasing systemic vascular resistance
• Reduced organ blood flow caused by vasoconstriction and reduced arteriole pressure leads to systemic acidosis that is sensed by the chemoreceptors
• The chemoreceptor system further stimulates the sympathetic adrenergic system thereby reinforcing the baroreceptor reflex

Question 24

Describe the humoral compensatory responses to changes in arterial pressure

Answer 24

• Sympathetic stimulation of the adrenal glands stimulates the release of catecholamines (i.e. epinephrine) into the blood which reinforces the effects of sympathetic activation on the heart and vasculature
• When blood loss occurs, the kidneys will release more renin following hemorrhage which leads to increased circulating levels of angiotensin II and aldosterone
• This causes vasculature constriction, enhanced sympathetic activity, stimulation of vasopressor release, activation of the thirst mechanisms and very importantly increased renal reabsorption of sodium and water to increase blood volume

Question 25

What are the clinical manifestations of shock in the respiratory system?

Answer 25

- rapid, shallow respirations (tachypnea) - respiratory rate increases as the oxygen-carrying capacity of the blood decreases Newborn to 2 months: 60 breaths per minute Infant 2 months to 1 year: 50 breaths per minute Preschool Child 1 to 5 years: 40 breaths per minute School age Child: 20-30 breaths per minute Adults: 20 breaths per minute

Question 26

What are the clinical manifestations of shock in the cardiovascular system?

Answer 26

a) Tachycardia - pulse rate ↑ (SNS stimulation) - tachycardia occurs to maintain CO and MAP when the blood’s circulating volume is declining ``` Tachycardia Newborn to 3 months: 190 bpm Infant 3 months to 1 year: 160 bpm Preschool Child 1 to 5 years: 120-130 bpm School age Child: 110 bpm Adults: 100 bpm ``` b) Hypotension - SBP indicates the integrity of the heart, arteries and arterioles - DBP dictates the resistance of the blood vessels - usually BP begins to ↓ when total blood volume is decreased 15-20% - as shock progresses, the SBP & DBP ↓; SBP drops more than the diastolic - pulse pressure narrows ``` ypotension 1. Adults: BP < 90/60 Pediatrics * no set values (calculations based on numerous factors); general guidelines for blood pressure values indicating the need for fluid resuscitation: Newborn SPB <50 mm Hg Infant SPB <60 mm Hg Child SBP <70 mm Hg ```

Question 27

What are the clinical manifestations of shock in the neuroendocrine system?

Answer 27

- In early shock, hyperactivity of the SNS causes the patient to feel anxious, nervous, and irritable - LOC decreases as circulation to the brain tissue becomes impaired – may cause confusion, agitation, restlessness - Lack of blood to brain may lead to dizziness, fainting, unconsciousness

Question 28

What are the clinical manifestations of shock in the renal system?

Answer 28

- earliest manifestation of shock is decrease in urinary volume - urine output should be kept greater than 0.5 ml/kg/hr - urinary flow of less than 0.5ml/kg/hr can cause ATN (acute tubular necrosis) from inadequate renal circulation *Normal urine output is age-dependent. Urine output should be 0.5-1ml/kg/hr in an adult (infant: 2mL/kg/hr; preschooler: 1.5mL/kg/hr; school-age: 1mL/kg/hr). Minimum urine output in adults should be at least 30mL/hr; oliguria is considered as <500mL per day.

Question 29

What is the mnemonic to remember the clinical manifestations of shock?

Answer 29

``` C – Cardiac output decreased H - Hypotension O - Oliguria R – Rapid, shallow breathing D – Drowsiness, confusion, decreased LOC ``` I - Irritability T - Tachycardia E – Extremities cool, clammy skin M – Multi-organ damage

Question 30

What are the different types of shock?

Answer 30

- Hypovolemic - Vasogenic (anapylactic, neurogenic, and septic) - Obstructive - Cardiogenic

Question 31

What is hypovolemic shock?

Answer 31

- Caused by a loss of blood, plasma or extracellular fluid - Most common type of hypovolemic shock is hemorrhagic - Hypovolemic shock begins to develop when the intravascular volume has decreased by approx. 15% - Clinical manifestations: high systemic vascular resistance, poor skin turgor, thirst, oliguria, rapid heart rate, elevated RR, altered LOC, eventual low BP - Mortality rate from hemorrhagic shock ranges from 10-31% - Most common type of shock in children

Question 32

What is obstructive shock?

Answer 32

- Results from a mechanical obstruction to blood flow -> ↓ CO -> ↓ tissue perfusion - The intravascular volume is sufficient, but the obstruction is preventing normal circulation of the blood - Causes of obstructive shock include: Tension pneumothorax; pericardial tamponade; pulmonary embolism; superior vena cava syndrome; abdominal compartment syndrome - Clinical manifestations: tachycardia, tachypnea, hypotension, jugular venous distension, low CO, cyanosis, skin mottling, rapid/faint/irregular pulses, low urine output, occasional peripheral edema

Question 33

What is cardiogenic shock?

Answer 33

- Occurs when the heart is unable to pump enough blood to meet the body’s demand for oxygen - Results in persistent hypotension and tissue hypoperfusion despite adequate vascular volume - #1 cause of cardiogenic shock is myocardial infarction - Other causes include: structural damage to the heart; damage to the valves of vessels; dysrhythmias; CHF; valvular pathology - Subjective symptoms: chest pain, dyspnea, faintness, feelings of impending doom - Clinical manifestations: tachycardia, tachypnea, hypotension, jugular venous distension, low CO, cyanosis, skin mottling, rapid/faint/irregular pulses, low urine output, peripheral edema

Question 34

What is vasogenic shock?

Answer 34

- Even though the 3 types of vasogenic shock have different etiologies, they all cause a similar physiologic response - Vasogenic shock results in: impaired SVR, maldistribution of blood flow, and altered organ perfusion - Although the intravascular volume remains normal in vasogenic shock, a functional or relative hypovolemia occurs

Question 35

Describe neurogenic shock

Answer 35

- Results from extreme, persistent vasodilation - In neurogenic shock, the blood volume has not changed but the amount of space containing the blood has increased - This massive vasodilation results in a dramatically decreased SVR - The pressure in the vessel walls is no longer adequate to drive nutrients across capillary membranes - Neurogenic shock can be caused by any factor that stimulates parasympathetic activity or inhibits sympathetic activity - Causes include: trauma to the spinal cord or medulla, certain depressive drugs, anaesthetic agents and severe emotional distress or pain - Clinical manifestations: low SVR, bradycardia, warm skin temperature and normal or flushed skin, hypotension

Question 36

Describe neurogenic shock in terms of a step-by-step process

Answer 36

An imbalance between the parasympathetic (overstimulated) and sympathetic (understimulated)nervous system -> massive vasodilation -> decreased vascular tone -> decreased systemic vascular resistance -> inadequate cardiac output -> decreased tissue perfusion -> impaired cellular metabolism

Question 37

What is anaphylactic shock?

Answer 37

- Is the outcome of a widespread hypersensitivity reaction known as anaphylaxis - Often more severe than other forms of shock because the hypersensitivity reaction causes widespread vasodilation but also other pathophysiologic effects that rapidly involve the entire body - Cardiovascular collapse and airway compromise - The invading allergen causes an extensive immune and inflammatory response that results in vasodilation and increased vascular permeability - Although this immune and inflammatory response causes vasodilation, it also, conversely, results in constriction of the extravascular smooth muscle = respiratory difficulties - The onset of anaphylactic shock is usually sudden and progression to death can occur within minutes - Resolution may begin when treatment is given, but may take up to 24 hours - Potential for second phase reactions (biphasic reaction) - Clinical manifestations: anxiety, difficulty breathing, cough, stridor, nausea/vomiting, diarrhea, abdo pain, flushing, urticaria, edema, decreased LOC, decreased SVR, hypotension, tachycardia, tachypnea, oliguria, cardiac/respiratory arrest

Question 38

What is septic shock?

Answer 38

- Septic shock is the result of infection that overwhelms the host defenses - 6 most common infection sites/causes: pneumonia, bloodstream, intravascular catheter, intra-abdominal, urosepsis, surgical wound infection - Can be caused by gram negative/positive bacteria and fungi - Prognosis is significantly affected by the source and virulence of the infectious microorganism - Invading organism migrates into the bloodstream and releases toxins triggering a massive inflammatory response - This causes maldistribution of blood flow, vasodilation, depression of myocardial contractility and damages the capillaries, this increases capillary permeability and results in fluid leaking out of the vascular space - This results in hypotension and tissue hypoperfusion - Clinical manifestations: persistently low BP, low SVR, tachycardia, temperature instability (hyper/hypothermia), decreased LOC, tachypnea, nausea/vomiting/diarrhea, high or low WBC

Question 39

What is multiple organ dysfunction syndrome?

Answer 39

- progressive dysfunction of 2+ organ systems due to an uncontrolled inflammatory response - Can progress to organ failure and death - Occurs during severe sepsis as well as with other severe illnesses/injuries - Leading cause of mortality in surgical ICUs - Morality 54% (with 2 failing organ systems) ranging to 100% (with 5 failing organ systems) - Prevention is key! - Treatment consists of supportive measures

Question 40

What are the phases of shock?

Answer 40

1. Initial 2. Compensatory 3. Progressive 4. Irreversible 5. Death

Question 41

Describe the initial phase of shock

Answer 41

- The symptoms are almost imperceptible - Pulse rate and blood pressure may decrease slightly and the skin may be pale, cool and moist - Cells begin to change due to issues with perfusion and oxygenation - Anaerobic metabolism -> lactic acid and pyruvic acid

Question 42

Describe the compensatory phase of shock

Answer 42

- Compensatory mechanisms aim to preserve organ perfusion at the expense of integumentary and intestinal perfusion - In this phase the actual or perceived loss of vascular volume stimulates the baroreceptors in the aortic arch and carotid sinus to stimulate the sympathetic nervous system to release catecholamines from the adrenal cortex and medulla - Catecholamines increase heart rate, increases SVR and BP, increase contractility of the heart, and increase CO - The posterior pituitary secretes ADH to stimulate reabsorption of water from the kidneys - The renin-angiotensin-aldersterone system is activated to increase sodium and water reabsorption Cortisol is secreted to increase mobilization of glucose

Question 43

What is the overall purpose of the compensatory mechanism? what are the clinical manifestations?

Answer 43

- The overall purpose of this response is to improve tissue perfusion and support cellular metabolism through 4 mechanisms: CO is improved Blood flow is increased to central essential organs Plasma volume is increased Gluconeogenesis - Clinical manifestations: anxiety, restlessness, pallor and decrease in peripheral skin temperature, slight increase in HR progressing to tachycardia, normal BP can be maintained for some time, reduced urine output

Question 44

Describe the progressive stage of shock

Answer 44

- This phase marks the exhaustion of the compensatory mechanisms - Hypotension is the hallmark clinical finding - Metabolic acidosis Acidosis and increased carbon dioxide causes microcirculation to dilate, lactic acidosis increases capillary permeability and relaxation of the capillary sphincters - Perfusion to the core organs is significantly compromised - Clinical manifestations: altered LOC, hypotension, hypothermia, anuria

Question 45

Describe the irreversible phase of shock

Answer 45

- Ongoing hypoperfusion results in irreversible cellular and organ damage (necrosis) - Markedly increased lactate levels and severe acidosis - Hallmark of this phase is the predictable progression of organ system dysfunction and eventually death - Once the cells in organs begin to die, the organ ceases to function and the other organs will follow suit – leading to multiple organ failure which will lead to death

Question 46

What is the goal of treatment? What does the treatment and management of shock generally include?

Answer 46

Overall goal of treatment is to reverse the primary cause and restore oxygen delivery to the tissues Treatment & management generally include: - Maintaining an airway - Respiratory/cardiac assessments - Regular vitals (Q5 min for critical patients) - Labs & diagnostics - 100% oxygen - Circulatory support - Fluid resuscitation

Question 47

How do you treat hypovolemic shock?

Answer 47

- Early identification - Treat the cause (i.e. control hemorrhage, restore circulating volume) - Optimize O2 delivery

Question 48

How do you treat obstructive shock?

Answer 48

- Early identification - Treat the cause - Supportive care (ex. O2 therapy)

Question 49

How do you treat cardiogenic shock?

Answer 49

- Early identification - Treat the cause (i.e. re-establish circulation to the myocardium) - Supportive care (i.e. O2 therapy and airway support, cardiac drugs, fluid resuscitation)

Question 50

How do you treat neurogenic shock?

Answer 50

- Early identification - Fluid replacement for BP or changes in LOC (BP < 90, UO < 30cc/hr) - Other supportive care: medications (ex. vasopressors, steroids, atropine) ventilatory support

Question 51

How do you treat anaphylactic shock?

Answer 51

- Early identification - Epinephrine - Supportive care: airway support, fluid resuscitation, medications (i.e. antihistamines, corticosteroids)

Question 52

How do you treat septic shock?

Answer 52

- Early identification - Fluid resuscitation - Antibiotics - Other supportive care: medications (i.e. vasopressors, inotropic drugs, O2 therapy, heparin for DIC, nutritional support)

Question 53

What are the goals of nursing management of shock?

Answer 53

- Correct the causative factor - Improve oxygenation - Restore and maintain adequate perfusion - Prevent complications

Question 54

What does the assessment consist of in shock?

Answer 54

1. History of causative and risk factors from the client 2. Fluid intake and output for past 24 hrs 3. Signs of covert bleeding 4. Mental status changes 5. Cardio vascular status 6. Respiratory status

Question 55

How can you improve oxygenation in nursing management?

Answer 55

- look for airway or breathing problems - check airway patency - assess respiratory rate and effort

Question 56

How can you restore and maintain adequate perfusion in nursing management?

Answer 56

- assess pulse, BP, skin colour, temperature, heart sounds, peripheral pulses, state of hydration, and skin perfusion (cap refill) - check condition of mucous membranes, sclera, and conjunctiva for pallor or cyanosis - assess fullness of neck veins (JVD), may suggest right heart failure - IV therapy

Question 57

How can you monitor for complications in nursing management?

Answer 57

- SBP decreased more than 20 mmHg with HR increased more than 20 BPM indicates actual or relative hypovolemia requiring immediate assessment of need for fluid replacement and CV support. - Decreased O2 sats and respiratory distress also require immediate intervention - Decreased UO (< 30ml/hr)

Question 58

What nursing care actions can be taken when managing shock?

Answer 58

1. Keep patient warm: in supine position 2. Monitor hemodynamic status and vital signs 3. Monitor urine output and specific gravity 4. Reduce patient’s anxiety 5. Administer intravenous fluids and medications as ordered 6. Monitor oxygen saturation and provide oxygen therapy as indicated

Question 59

What nursing evaluation can be taken when managing shock?

Answer 59

1. Maintains stable hemodynamic status 2. Maintains a urine output – 30ml per hour 3. Remains oriented to time, place and person 4. Maintains adequate cardiac output.