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NUR3310 > Shock > Flashcards

Shock Flashcards

1
Q

Define ‘shock’

A

a potentially life threatening syndrome characterised by inadequate tissue perfusion, resulting in impaired cellular respiration and functioning

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2
Q

Define healthy tissue perfusion

A

cells can use the oxygen to convert glucose to energy (ATP). This ATP is then used by the cells to carry out their metabolic activities. The process is called cellular respiration
adequate oxygen perfusion allows for aerobic metabolism, inadequate oxygen perfusion becomes anaerobic metabolism

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3
Q

What is the difference between aerobic metabolism and anaerobic metabolism?

A

aerobic is efficient and produces 36 units of ATP (energy), opposed to anaerobic metabolism, which produces only 2 units of ATP and produces lactic acid which harms cells

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4
Q

What is the cellular respiration equation?

A

C6H12O6 + 6O2 –> 6CO2 + 6H2O + ATP (36 molecules)

Glucose + Oxygen –> Carbon Dioxide + Water + Energy

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5
Q

Outline the effect of impaired oxygen perfusion on the body

A

impaired oxygen -> anaerobic metabolism triggered -> decreased ATP production -> loss of cell membrane permeability -> NA+/K+ pump lost -> fluid shifts -> lysosomal enzymes released -> cellular death and organ failure

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6
Q

Outline the effect of impaired glucose on the body

A

impaired access to and use of glucose by the cell -> access other sources of energy -> increasing acidosis -> protein depletion -> impaired cellular metabolism

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7
Q

What are the three stages of shock?

A

Compensatory stage, progressive stage, and irreversible/refractory stage

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8
Q

Define the compensatory stage of shock

A

Compensatory mechanisms activated:
>decreased CO stimulates receptors
>Adrenaline and noradrenaline released
Blood flow to most essential organs (heart & brain) maintained
>decreased blood flow to kidneys, GIT, lungs and skin
>renin-aldosterone system activated
>antidiuretic hormone (ADH) released
If corrected patient can recover from this stage

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9
Q

Define the progressive stage of shock

A

Compensatory mechanisms fail
Decreased ATP production, Hypoxia of vital organs, Decreased cellular perfusion and tissue ischemia, Metabolic acidosis, Decreased cardiac output, Myocardial ischemia. Increased risk of gastric trauma, Increased risk of developing disseminated intravascular coagulation (DIC) (abnormal clotting), Acute renal failure
Aggressive management required to prevent multiple organ dysfunction syndrome (MODS)

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10
Q

Define the irreversible/refractory stage of shock

A

Compensatory mechanisms are overwhelmed
Severe tissue hypoxia with ischemia, necrosis and death of the cell occurs
Build up of toxins
Multi-organ failure
Recovery unlikely

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11
Q

What are the four types of shock?

A

Hypovolaemic shock (loss of intravascular volume)
Cardiogenic shock (pump failure)
Distributive shock (systemic vasodilation)
Obstructive shock (physical obstruction of blood circulation)
These can occur in isolation or in combination (Multifactorial shock)

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12
Q

What are the three types of Distributive shock?

A

Septic shock (infection), anaphylactic shock (allergic reaction), neurogenic shock (spinal cord injury potential complication)

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13
Q

Outline hypovolaemic shock

A

Caused by a loss of fluid. This can be from whole blood (haemorrhage), plasma (burns) or interstitial fluid (vomiting, diaphoresis). Shock begins to develop when the total circulating volume is decreased by approximately 15%

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14
Q

What are clinical manifestations of hypovolaemic shock

A

anxiety, tachypnoea, hypotension (may be HTN at first due to compensatory measures), tachycardia, weak peripheral pulses, clammy moist skin, thirst, acidosis

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15
Q

Outline cardiogenic shock

A

occurs from cardiac pathology causing inadequate cardiac output leading to tissue hypoxia. Cardiogenic shock occurs in the presence of ADEQUATE intravascular volume
Causes include reduced contractility, inadequate filling, arrhythmia, and failure of forward flow

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16
Q

What are clinical manifestations of cardiogenic shock?

A

increased WOB, elevated RR, crackles/acute pulmonary oedema (APO), tachycardia, hypotension, distended neck veins, clammy skin, prolonged cap refill, decreased urine output, confusion

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17
Q

Define distributive shock

A

results from excessive vasodilation and impaired distribution of blood flow.
There are three types of distributive shock: Septic shock, Anaphylactic shock, Neurogenic shock

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18
Q

Define septic shock

A

Occurs when a patient develops sepsis: a life threatening condition of bacteria has entered in the bloodstream which triggers an inflammatory response.
Septic shock will develop when this response causes widespread vasodilation, tachycardia, decreased myocardial contractility and decreased tissue perfusion

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19
Q

What are clinical manifestations of septic shock?

A

Tachypnoea, Hypoxia, Hypotension, Systemic oedema, Tachycardia, febrile, Decreased urine output, Hot clammy skin, Confusion

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20
Q

Outline anaphylactic shock

A

anaphylaxis is reportable to the government
Anaphylactic shock is a result of a systemic hypersensitivity reaction. The patient has an antigen-antibody response. A large number of inflammatory mediators are released. This causes there to be a gross immune and inflammatory response. The symptoms are often sudden and severe
anaphylactic shock can be acutely fatal if smooth muscle contraction of the airways occurs

21
Q

What are clinical manifestations of anaphylactic shock?

A

Angioedema (swelling of the deeper layers of the skin, caused by a build-up of fluid), Stridor (wheezing), Dyspnoea, Bronchospasm and wheeze, Hypotension and cardiovascular collapse, Abdominal cramps, Diarrhoea, Flushing or pallor, Urticaria (hives), Coagulopathy

22
Q

Outline neurogenic shock

A

Occurs when sympathetic vascular tone is lost; from severe injury to the nervous system.
An imbalance occurs between the sympathetic and parasympathetic stimulation of vascular smooth muscle and this results in massive vasodilation without compensation

23
Q

What are clinical manifestations of neurogenic shock?

A

Hypotension, Bradycardia, Hypothermia

24
Q

Outline obstructive shock

A

occurs when a blockage or disruption of a major vessel in the systemic, pulmonary or circulatory systems occurs and interferes with cardiac output. Stroke volume is reduced, leading to a decrease in cardiac output, inadequate tissue perfusion and impaired cellular metabolism
common causes are: cardiac tamponade, tension pneumothorax, pulmonary embolisms

25
Q

What are some examples of cardiogenic shock?

A

AMI (acute myocardial infarction AKA heart attack), cardiomyopathy (heart muscle disease)

26
Q

What are some examples of hypovolaemic shock?

A

trauma, gastroenteritis (acute GIT inflammation leading to vomiting & diarrhoea)

27
Q

What are some examples of distributive shock?

A

Sepsis, anaphylaxis

28
Q

What are some examples of obstructive shock?

A

PE (blood clot prevents blood flow to the lungs), cardiac tamponade (fluid build-up in pericardial sac)

29
Q

What is the relation ship between hypovolaemic shock and fluid loss?

A

patients can compensate for losses of up to 15%
15-30% -> SNS activated, increased HR, CO and RR
>30% - compensatory mechanisms begin to fail
>40% - irreversible tissue damage occurs

30
Q

What is the pathophysiology of hypovolaemic shock?

A

decreased blood volume -> decreased venous return -> decreased stroke volume -> decreased cardiac output -> decreased tissue perfusion

31
Q

What are some causes of hypovolaemic shock?

A

External fluid losses: trauma, vomiting/diarrhoea, diabetes, diuresis
Internal fluid losses: dehydration, burns, ascites, peritonitis

32
Q

What are some management considerations for hypovolaemic shock?

A

Provide oxygen therapy, assess for source of fluid loss, control external bleeding/fluid loss, IV fluid therapy, assess BGL, prevent hypothermia, consider blood products if required

33
Q

What is the pathophysiology of anaphylactic shock?

A

allergen -> release of vasoactive mediators ->
1. massive vasodilation -> hypovolaemia
2. increased capillary permeability -> fluid shifts to interstitial space -> widespread oedema -> respiratory distress/airway obstruction

34
Q

What are some management considerations for anaphylactic shock?

A

remove source of anaphylaxis if possible (eg. IV infusion)
assess for level of consciousness, monitor for airway compromise: drooling, swelling, wheezing ect. Suction/nebulised adrenaline/prepare for intubation or tracheostomy if needed
Provide oxygen/bronchodilators/corticosteroids if needed
consider fluid resuscitation, provide adrenaline, may need to consider vasopressors

35
Q

Outline anaphylactic shock management via adrenaline

A

Child >12 years = 500mcg IM adrenaline
Child 6-12years = 300mcg IM adrenaline
Child <6 years = 150mcg IM adrenaline
(repeat dose after 5 mins)

36
Q

Outline Anaphylaxis management

A

ASSESS FOR: upper airway obstruction (stridor, oral swelling), lower airway obstruction (wheeze, respiratory distress), shock (dizziness, pale, clammy)
CALL FOR HELP
CARDIAC ARREST?
if YES - begin basic life support
if NO- Adrenaline IM: adults 0.5mg, child 10mcg/kg
repeat every 5 mins as needed
Attach cardiac monitering, high flow oxygen, and place IV access
(for SHOCK: 0.9% saline rapid infusion - 1000ml adults, 20mL/kg children)
Consider -> further saline, nebulised adrenaline, adrenaline infusion, nebulised salbutamol

37
Q

What are risk factors for septic shock?

A

Age (<1 year - >65 years), malnutrition, chronic medical conditions, traumatic injury, invasive devices, wounds, surgery

38
Q

What are some management considerations for septic shock?

A

remove routes of infection, optain path samples, strict asepsis, control hyperglycaemia, broad spectrum antibiotics, temperatur regulation, treat symptoms
fluid resuscitation, monitor response, Central venous access if required

39
Q

Outline initial resuscitation for septic shock

A

MEDICAL EMERGENCY
1. measure lactate level (remeasure if elevated >2mmol/L)
2. obtain blood cultures
3. administer broad spectrum antibiotics
4. begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate >4 mmol/L
5. apply vasopressors if hypotensive during or after fluid resuscitation to maintain mean arterial pressure >65mmHg (MAP)

40
Q

What causes cardiogenic shock?

A

ineffective forward motion of blood

41
Q

what is the pathophysiology of cardiogenic shock?

A
  1. ineffective ventricular emptying -> increased pulmonary pressures -> pulmonary oedema -> decreased oxygenation
  2. decreased stroke volume -> decreased cardiac output
    = decreased cellular oxygen supply -> ineffective tissue perfusion -> impaired cellular metabolism
42
Q

Outline management of cardiogenic shock

A

secure airway if needed, monitor airway, assess for tachycardia/arrhythmias, hypotension, cool clammy skin. improve cardiac function via mechanical or inotropes (drugs that tell your heart muscles to beat or contract with more power or less power- eg. adrenaline/noradrenaline)
Check BGLs

43
Q

What is the pathophysiology of obstructive shock?

A

structural compression -> reduced venous return -> reduced stroke volume -> reduced cardiac output -> reduced tissue perfusion -> reduced oxygen availability to cells = impaired cellular metabolism

44
Q

Outline the primary goal of obstructive shock management

A

to identify and relieve the cause of the block
Eg. decompression for a tension pneumothorax, chest drain for a hemopneumothorax, thrombolytic therapy for a PE

45
Q

Define a central venous catheter

A

a long catheter inserted under sterile technique with local anaesthetic.
It is inserted into a large vein until the tip reaches the superior vena cava (near the right atrium of the heart)
Most commonly used veins: subclavian, internal, jugular, external jugular, femoral (less common)

46
Q

What are indications for a CVC?

A

Administer large volume of fluids, Long term access, Multiple drug administration, Administer irritating medications, Administer total parenteral nutrition (TPN), Difficulty obtaining other access, Provide access for transvenous pacing or pulmonary artery (PA) catheter

47
Q

List some examples of CVCs

A

hickmans, port-a-cath, PICC

48
Q

What are potential complications for a CVC?

A

During insertion: Pneumothorax, Haemothorax, Air embolus, Arterial cannulation, Incorrect positioning, Arrhythmia, Cardiac injury, Bleeding, Nerve injuries
Post insertion: Haemorrhage, Subcutaneous emphysema, Thrombosis, Sepsis, Infection, Extravasation

49
Q

Outline nursing considerations for a CVC

A

Check integrity regularly, infusions must be done via pump, flush all ports that are not in use, ensure dressing is intact, assess for signs of infection, dont do BP on an arm with a PICC insitu, sterile technique must be used

NUR3310 (9 decks)

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