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NSB236 > Week 1: Shock > Flashcards

Week 1: Shock Flashcards

1
Q

What is shock?

A

Shock is a state of insufficient perfusion and oxygenation delivery to vital organs and tissues through the body.

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2
Q

What are the main treatment strategies for shock?

A

Addressing perfusion deficiencies - increase O2 delivery cells (cellular hypoxia occurs secondary to impaired perfusion and increased cellular consumption of O2).

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3
Q

What is the difference between ventilation, oxygenation and perfusion?

A

Ventilation = The provision of fresh air to a room, or building

Oxygenation = the addition of oxygen to any system, including the human body.

Perfusion = is the passage of fluid through the circulatory system or lymphatic system to an organ or a tissues, usually referring to the delivery of blood to a capillary bed in tissue.

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4
Q

What is the pathophysiology of shock?

A

Perfusion is inadequate to sustain normal cellular metabolism - cellular hypoxia and cell death.
Shock is triggered by a sustained decrease in Mean Arterial Pressure which adversely impacts on and leads to a decrease in cardiac output, circulating blood volume and vascular dilation.

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5
Q

What is the Haemodynamic concept associated with shock?

A

Mean Arterial Pressure (MAP) is the perfusion pressure within the arteries during one cardiac cycle - provides a better indicator of perfusion to organs.
MAP = [SBP + (2xDBP)]/3
e.g. BP128/78 - [128+(2x78=156)]/3 - 284/3 = 95mmHg

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6
Q

What are the haemodynamic core principles?

A

Study of forces involved in blood circulation.
Four cardiovascular properties are necessary to maintain adequate tissue perfusion for cellular metabolism:
1. Sufficient CO (CO = SVxHR)
2. Uncompromised vascular tone
3. Sufficient blood volume and pressure
4. Tissues are able to utilise oxygen

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7
Q

What are some possible causes of a wide pulse pressure?

A
  • Atherosclerosis
  • Hyperthyroidism
  • Increased ICP
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8
Q

What is the result of a low pulse pressure?

A

<25% of the systolic value - insufficient preload, heart failure, shock state.

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9
Q

What is the normal range of Central Venous Pressure (CVP)?

A

2-8mmHg

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10
Q

What is Central Venous Pressure (CVP) and how is it measured?

A

It is a measure of preload.

CVP measure is taken above the right atrium using a central venous catheter.

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11
Q

When is Central Venous Pressure (CVP) measuring necessary / applied within nursing?

A
  • Pt with hypotension who isn’t responding to basic clinic management.
  • Continuing hypovolaemia secondary to major fluid shifts or loss
  • Pts requiring infusion of vasoactive agents (e.g. inotropes and vasopressors)
Inotropes = medication that either increases or decreases cardiac contractility i.e. adrenaline
Vasopressors = agents that cause vasoconstriction i.e. noradrenaline.
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12
Q

How much O2 do cells consume?

A

25%

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13
Q

Explain Oxygen delivery (include physiology)

A

The bodies ability to provide O2 to the cells is O2 delivery.
During physiological stress consumption is dependent on delivery and initially compensatory responses occurs such as increase HR.
If cells cannot extract enough O2 for energy then anaerobic metabolism occurs.

Inefficient energy production system = lactic acid.
If O2 delivery continues to be insufficient to meet cellular O2 consumption requirements = cell death - tissue ischaemia and dysfunction.

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14
Q

What are the 3 Neurohormonal Compensatory Mechanisms?

A
  1. SNS Activation
  2. Neuroendocrine response
  3. Renin-Angiotensin Aldosterone System Activation (RAAS).
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15
Q

What is SNS Activation?

A
  • baroreceptor stimulation = SNS nerves & adrenal medulla stimulated = catecholamine’s released = systemic vasocontriction = + HR and myocardial contractility = + CO & BP
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16
Q

What is the Neuroendocrine response?

A
  • arterial pressure = stimulates ADH secretion from pituitary = vasocontriction = + SVR, BP and venous return (preload) = + CO
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17
Q

What is Renin-Angiotensin Aldosterone System Activation

A
  • renal perfusion & + SNS stimulation = renin released to stimulate angiotensin 1 = converted to angiotensin 2 by ACE = arteriolar constriction & aldosterone release by adrenal cortex = kidneys conserve Na+ and H2O = + preload
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18
Q

What are the 3 compensatory response mechanisms to maintain effective blood volume in shock?

A
  1. Vasoconstriction
  2. Decreased renal losses of fluid
  3. Fluid re-distribution to the vascular space
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19
Q

What is a compensatory mechanisms to optimize cardiac performance during shock?

A

Increased HR & contractility (inotrophy, chronotrophy, dromotrophy).

20
Q

What are 2 compensatory mechanisms that preferentially maintain perfusion of vital organs during shock?

A
  1. Extrinsic regulation of system arterial tone

2. Auto-regulation of vital organs (brain, heart, kidneys).

21
Q

What are things to consider in regards to shock in infants?

A
  • Developing immune system
  • Large body surface area
  • Infants and children compensate very well
  • Dropping BP is a late sign of shock in this population
  • O2 & glucose dependant
22
Q

What are signs of shock (hypoperfusion) in infants?

A
  • Apathy or lack of vitality
  • Rapid RR
  • Rapid or weak and thready pulse
  • Delayed capillary refill
  • Falling BP
  • Absence of tears when crying
  • Pale, cool, clammy skin
  • Altered mental status
23
Q

What are the 3 main considerations associated with shock in the elderly?

A
  1. Cardiovascular
  2. Respiratory
  3. Hematologic and immune system.
24
Q

Why should the cardiovascular system be considered for shock in the elderly?

A
  • Left ventricular myocardial thickening
  • Decreased responsiveness to SNS
  • Stiffening of arterial vessels and heart valves
25
Q

Why should the respiratory system be considered for shock in the elderly?

A
  • Decreased muscle strength and elastic recoil
  • Decreased alveolar surface area
  • Increased resting RR
26
Q

Why should the hematologic & immune system be considered for shock in the elderly?

A
  • Decreased blood cell production in the marrow
  • Increased incidence of anaemia
  • Decreased immune function
27
Q

What are the different classifications of shock?

A
  1. Cardiogenic (pump failure)
  2. Hypovolaemic (fluid volume loss)
  3. Distriblutive (fluid volume redistribution = septic, anaphylactic, neurogenic)
28
Q

What is the pathophysiology of cardiogenic shock?

A

Decline in CO contributing to tissue hypoxia despite adequate circulating volume.

29
Q

What are the causes of cardiogenic shock?

A
  • AMI (left ventricular failure - most common)
  • Severe MV regurgitation
  • Cardiac tamponade
  • Cardiomyopathies
  • Post cardiac surgery
30
Q

What is the treatment of cardiogenic shock?

A
  • Improve O2 delivery by decreasing demand
  • Re-establish blood flow (if feasible)
  • Pharmacological agents aimed at controlling HR, antiarrhythmic, reduce preload and afterload, inotropes, coronary artery dilators.
31
Q

What are the primary pharmacological interventions provided to shock Pt’s?

A
  • Beta Blockers (hypotenstion)
  • Antiarrhythmic (digoxin [cardiac glycoside], amiodarone)
  • Loop diuretic (frusemide)
  • Inotrope (dobutamine)
  • Vasopressors (noradrenaline)
32
Q

What is the pathophysiology of hypovolaemic shock?

A

Inadequate circulating volume due to blood and / or fluid loss.

33
Q

What causes hypovolaemic shock?

A
  • Sustained vomiting / diarrhoea
  • Severe dehydration
  • Surgery
  • Fluid shifts (3rd spacing from burns/ascites)
  • Haemorrhage
34
Q

What is the treatment for hypovolaemic shock?

A
  • Address primary cause (e.g. bleeding, burns)
  • Fluid replacement (+/- warm fluids)
  • Optimise oxygenation
  • Monitor CVP
  • Lactate (hypoperfusion and reduce O2 delivery)
35
Q

What is the pathway continuum of septic shock?

A

Systemic Inflammatory Response Syndrome (SIRS) = Sepsis (SIRS & infection) = Severe sepsis (sepsis & end organ damage) = septic shock (severe sepsis & hypotension)

36
Q

Who are the at risk Pts with distributive/septic shock?

A
  • Advancing age
  • Immunocompromised
  • Chronic diseases
  • Invasive instrumentation/surgery
  • Malnutrition
  • Sequential infection treated with broad spectrum A/B
37
Q

What is needed to maintain BP & MAP in distributive/septic shock?

A

Inotropes / vasopressors to maintain BP + MAP

38
Q

What do you need to watch out for in Pts with distributive / septic shock?

A
  • Pts who do not get a febrile response even though septic.
  • Pts who do not man a WCC response to an infection
  • Pts who suddenly drop their BGLs
39
Q

What is the clinical management of septic shock?

A
  1. Early administration of IV antibiotics (broad spectrum). Consider clinically if you need to monitor blood levels for A/B and their impact on renal functions.
  2. Correct hypoperfusion - with at least 30mL/Kg of crystalloid and additional fluids as guided by haemodynamic assessment (BP, MAP, CVP/JVP, UO, lactate, CRT- peripheral perfusion.
  3. MAP >65mmHg - vasopressor may be required if not responding to fluids
  4. Oxygen delivery = cellular hypoxia takes time to correct. Consider Pt positioning
  5. Renal output = may be adversely effected due to hypoperfusion (minimum urinary output 0.5mL/Kg/Hr - monitor urea, creatinine & GFR).
  6. Monitor BGLs irrespective of Hx (+catabolism).
  7. Monitor skin integrity (observe for bruising, coagulopathy)
  8. Consider consulting senior medical team or referrals of care
  9. Nutrition (+ metabolic demand and catabolic status - need dietician)
  10. GIT (monitor bowel sounds as may be impacted due to decreased perfusion)
  11. VSS
  12. Blood pathology
  13. Mobility (physio, risk of DVT)
  14. Psychosocial impacts (family, pets)
40
Q

What is severe anaphylactic shock?

A

Severe hypersensitivity to an allergen.
Antibody = antigen reaction causes immune response
Profound vasodilation causes maldistribution of blood to tissues = - preload & CO
+ capillary permeability causes loss of vascular volume = worsening CO & tissue perfusion

41
Q

What is the treatment for distributive / anaphylactic shock?

A
  • Adrenaline
  • Bronchodilators
  • Antihistamine
  • Corticosteroids
  • Fluids
  • Education
42
Q

What is distributive / neurogenic shock?

A

Imbalance between parasympathetic & sympathetic stimulation of vascular smooth muscle.
Impaired sympathetic tone = peripheral vasodilation, -SVR, blood pools in venous system = -venous return, CO & - tissue perfusion.
Most common causes is spinal injury above T6 (other include spinal analgesia, emotional distress, pain).

43
Q

What are the clinical signs of distributive / neurogenic shock?

A
  • BP, skin is warm and dry, anxious, restless, lethargy, oliguria/anuria, - body temp.
44
Q

What is the treatment for distributive / neurogenic shock?

A

Spinal cord stabilisation, careful administration of fluids, inotropes/vasopressors, monitor for hypothermia.

45
Q

What is the care process for a deteriorating patient?

A 
A = airway (secured, compromised, at risk)
B = breathing (rate, WOB, paradoxical)
C= circulation (BP, MAP, CRT, CVP/JVP, palor)
D = Disability / Drugs (GCS, delirium, AWS)
E = Environment / electrolytes
?F = Family (communication, support, should they be present)

Essentials = oxygenation, ventilation, perfusion
* Early identification, monitoring, consultation, documentation

46
Q

How does shock evolve/progress?

A
  1. SHOCK:
    a) Low blood flow
    (hypovolaemic = haemorrage or trauma)
    (Cardiogenic = acute myocardial infarction, cardiomyopathy).

b) Maldistribution of blood flow
(Septic = pancreatitis, infection - sepsis)
(Neurogenic = spinal cord injury, narcotic overdose)
(Anaphylactic = multiple transfusion, sever allergic reactions)

  1. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME [SIRS]
    a) Mediator excess: cytokines (e.g. tumour necrosis, factor interleukins), oxygen, free radicals.
    b) Widespread endothelial injury and dysfunction
    c) Vasodilation and increaed capillary permeability
    d) Tissue oedema
    e) Neutrophil entrapment in microcirculation
  2. MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)
    a) Cardiovascular dysfunction
    b) Lung Dysfunction
    c) Gastrointestinal dysfunction
    d) Liver dysfunction
    e) CNS dysfunction
    f) Renal dysfunction
    g) Skin dysfunction

NSB236 (5 decks)

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