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Technician Course MOD D 2016 > Mod D Tech 13 Shock and Fainting > Flashcards

Mod D Tech 13 Shock and Fainting Flashcards

1
Q

Definition of shock

A

Insufficient perfusion of the tissues with blood carrying oxygen and nutrients causing anaerobic metabolism and thus metabolic acidosis

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2
Q

Shock

Name Factors effecting

A
  • Blood volume
  • Cardiac output
  • Functioning blood vessels
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3
Q

Name Risk factors for shock

A
  • Trauma
  • Pregnant patients
  • Elderly patients
  • Cardiac patients
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4
Q

Name Types of Shock

A

Cardiogenic shock

Neurogenic shock

Toxic/Septic shock

Anaphylactic shock

Anaphylaxis

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5
Q

Cardiogenic shock

A

•Impaired cardiac function due to a damaged myocardium from either an infarct, arrhythmia or tamponade.

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6
Q

Describe Hypovolemic shock

A
  • Reduced circulating volume
  • Fluid loss

•

Major causes

  • Haemorrhage
  • Burns & scalds
  • Diarrhoea & vomiting
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7
Q

Describe Neurogenic shock

A
  • Head injury
  • Transection of the spinal cord

Spinal shock

  • Loss of nervous control
  • Relative Hypovolaemic
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8
Q

Describe Toxic/Septic shock

A
  • Infection such as meningitis causes release of toxins causing arteriolar and capillary dilatation
  • Loss of venous tone
  • Mismatch between the circulating blood volume and increased capacity of the blood vessels
  • Relative hypovolaemia
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9
Q

Describe Anaphylactic shock what does it affect

A
  • Exposure to Antigen
  • Previous exposure to Antigen
  • Excessive Antigen/ Antibody reaction
  • Histamine released with systemic effect

•

Affecting:

  • Tissues
  • Respiratory function
  • Circulatory function
  • Mismatch between the circulating blood volume and increased capacity of the blood vessels

•

•Loss of fluid into tissues, causing sudden oedema

•

•Causes difficulties with airway if around the face and neck

•

•Histamine may also cause brochospasm preventing adequate pulmonary ventilation

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10
Q

Anaphylaxis

A
  • Anaphylaxis - hypersensitivity reaction
  • Anaphylactoid - similar reaction but not dependent on hypersensitivity
  • Manifestations and management similar
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11
Q

Causes for Anaphlaxic

A
  • Drugs (e.g. penicillin, aspirin, vaccines)
  • Food substances (e.g. peanuts, shellfish, eggs)
  • Venom (e.g. wasp stings, bee stings)
  • Almost any foreign substance can become an allergen
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12
Q

what is Anaphylaxis

A

A severe allergic reaction, often affecting the whole body

It often occurs when patients are exposed to an allergen to which they have become over sensitive.

When an allergen is reintroduced into the body, mast cells may vigorously react and release an overdose of histamine

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13
Q

what does Histamine do

A
  • Released by mast cells and basophils
  • Causes vasodilation and increased blood vessel permeability
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14
Q

Leukotrines

A
  • Produced by mast cells and basophils
  • Cause bronchoconstriction, an increase in blood vessel permeability and coronary vasoconstriction
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15
Q

Physiological effects of anaphalaxiis

A
  • Decreased coronary blood flow
  • •Systemic vasodilation
  • •Reduced cardiac output
  • Increased permeability of the blood vessels
  • Spasm and oedema of the bronchi
  • •Pulmonary vasoconstriction
  • •Laryngeal oedema
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16
Q

Clinical Signs & Symptoms of Anaphlaxis

A
  • Extreme dyspnoea (coughing, wheezing, prolonged sneezing)
  • •Tachycardia (often with arrhythmias)
  • •Hypotension
  • Warm, flushed skin
  • •Oedema (particularly facial)
  • •Nausea & Vomiting
  • •Abdominal cramps
  • Urticaria (hives)
  • Pruritis (itching)
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17
Q

Anaphylaxis facts and figures

A

•Hypovolaemia occurs quickly – 50% of blood plasma volume is lost in 10 – 15 minutes

•

•>50% of fatalities occur within the first hour

•

•75% of fatalities are due to asphyxia from airway obstruction or bronchoconstriction

•

•25% of fatalities occur as a result of circulatory failure and hypotension

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18
Q

things to consider /mangerment

A
  • Consider when compatible history of severe allergic-type reaction with respiratory difficulty and/or hypotension especially if skin changes present – firstly remove from source
  • Oxygen - high flow then maintain 94-98%
  • Stridor, wheeze, respiratory distress or clinical signs of shock
  • Epinephrine (adrenaline) 1:1000 solution i.m. Repeat every 5 minutes as clinically indicated
  • Consider Salbutamol for Bronchospasm resistant to IM Adrenaline.
  • If clinical manifestations of shock do not respond rapidly to drug treatment:
  • Consider paramedic assistance for administration of antihistamine (Chlorpheniramine), fluids and hydrocortisone if the call is more than 30 mins from the hospital
19
Q

What is Adrenaline 1:1000 (Epinephrine)

what type

what effects

A
  • A sympathomimetic drug
  • •Stimulates alpha and beta receptors
  • •Alpha effect – reverses vasodilation and reduces oedema
  • •Beta effect – causes bronchodilation, increase heart rate and strength of contraction. Suppresses histamine and leukotrine release
20
Q

Adrenaline 1:1000
side effects:

A
  • Tachycardia
  • •Angina
  • •Hypertension
  • •Ventricular arrhythmias
  • Anxiety
  • •Headache
  • •Cerebral bleeding
  • •Nausea & Vomiting
21
Q

Adrenaline dosage

A
22
Q

Salbutamol Dosage

A
23
Q

How does the body respond to shock?

Compensatory mechanisms

A

Abnormal fluid loss:

  • Stimulates the Sympathetic Nervous System
  • Increased heart rate
  • •Selective artery constriction to non vital organs
  • •Increased venous tone mobilises reserve blood volume & reduces circulatory capacity

Hormonal Regulation

  • RAA= Renin-angiotensin-aldosterone system
  • •Activated by baroreptors sensing lowered BP and reduced renal blood flow
  • Renin released by kidneys works as an enzyme and converts angiotensinogen (made in the liver) to angiotensin I.
  • •Angiotensin I in lungs with ACE (Angiotesin converting enzyme) produces Angiotensin II, a potent vasoconstrictor
  • Angiotensin II stimulates release of Aldosterone by adrenal cortex, which increases sodium and water reabsorption

•

•Epinephrine and Noradrenaline

–Increase heart rate

–Increase vascular tone

–•ADH = Antidiuretic Hormone, produced by Hypothalamus and released by pituitary gland in response to blood loss to cause vasoconstriction

•

24
Q

Hypovolaemic shock

how many stages

split in to what

A

Four Stages

Compensated and Decompensated

25
Q

Stage 1
(up to 15% blood volume loss

Signs and symptoms

A
  • Pale skin
  • •Capillary refill < 2 seconds
  • •Pulse up to 100 bpm
  • •Blood pressure - no change
26
Q

Stage 2

signs and symptoms

(15% - 30% blood volume loss)

A
  • Pale, cool, clammy skin
  • •Capillary refill > 2 seconds
  • •Pulse > 100 bpm
  • •Increased respiratory rate
  • •Blood pressure - normal systolic pressure but raised diastolic pressure
  • The body’s compensatory mechanisms are at their limit
27
Q

Stage 3
(30% - 40% blood volume loss)
signs symptoms

A
  • Anxiety, restlessness & agitation
  • Pulse > 120 bpm
  • •Blood pressure - systolic pressure 100mmHg or less
  • The patient is in decompensated shock
28
Q

Stage 4
(> 40% blood volume loss)
signs and symptoms

A
  • Moribund appearance
  • •Central cyanosis
  • •Altered level of consciousness
  • •Pulse - weak with marked tachycardia
  • •Respiratory distress
  • •Blood pressure - systolic pressure 70mmHg or less
  • The patient is in critical condition
29
Q

Septic Shock

Definitions:

A

•Sepsis:- Presence of bacteria in the blood stream

•Septic shock:- Begins with the development of septicaemia usually from bacterial infections, but can be viral in origin.

This is the most common type of Distributive shock

30
Q

what is SIRS

A

Systematic Inflammatory Response Syndrome

The ‘normal’ response to injury doesn’t stop

The body develops SIRS

  • HR >90
  • RR >20 or ETCO2 <32mmhg (4.3kPa)
  • Temp <36c >38c
  • White cell count <4000 >12000

(normal range 4300 - 11,000 with both low and high counts can be attributed to bacterial infection)

•>10% immature neutrophils

31
Q

Stages of Sepsis how many

A
32
Q

Septic Shock

signs symptoms

A
  • Described as distributive shock reflecting the effects of the disease process on the movement of fluid around the different compartments of the body (Morton & Fontaine 2009)
  • Early symptoms of systemic vasodilation

i. red & flushed appearance
ii. full bounding pulse and rapid capillary refill
iii. increased peripheral circulation
iv. increased micro-vasculature permeability creating a major loss of volume from the core circulation (Jenkins et al. 2007)
v. Blood sugar levels increase to cope with the metabolic demands

33
Q

Recognition of Shock

General Signs & Symptoms

A
  • Increased pulse rate, becoming weaker
  • Hypotension
  • Pale, cool, clammy skin
  • Increased respirations becoming shallow
  • Nausea & vomiting
  • Thirst
  • Pupil reaction slow

Faintness & dizziness

34
Q

Signs & Symptoms
Spinal Shock

A
  • Loss of feeling
  • Pins & Needles
  • Paralysis
  • Displaced vertebrae / swelling
  • Fixation of spine
  • Priapism (men)
  • Hypotension
  • Normal Pulse
  • Normal colour above level controlled by point of transection
  • Warm & flushed below level controlled by point of transection
35
Q

Signs & Symptoms
Anaphylactic shock

A
  • Severe dyspnoea
  • Tachycardia
  • Severe hypotension
  • Warm, dry, flushed skin becoming pale as the condition worsens
  • Oedema
  • Itching
  • Nausea & vomiting

Abdominal cramps

36
Q

General management of shock

A
  • Safety
  • Do I need help
  • Ensure open airway
  • Oxygen to 94-98%
  • ? Assisted ventilation
  • Treat other injuries
  • Keep Pt. Temp. normal
  • Pt. Positioning (autotransfusion)
  • Reassurance
  • Monitor vital signs
  • Rapid / smooth transfer to hospital
  • Alert hospital using ATMIST
37
Q

Management of spinal shock

A
  • Safety
  • Do I need help
  • Ensure open airway
  • High conc. Oxygen
  • ? Assisted ventilation
  • Immobilise fractures
  • Control bleeding
  • Avoid unnecessary movement
  • Keep Pt. temp. normal
  • Reassurance
  • Monitor vital signs
  • Rapid / smooth transfer to hospital
  • Alert hospital using ATMIST
38
Q

Fainting or Syncope

Causes and Types

A
  • Postural fainting
  • •Emotional stress
  • •Cardiac origin
39
Q

Postural Fainting

A

•Standing quickly from a recumbent position

•

•Prolonged periods of standing particularly in hot weather

•

•Athletes may be vulnerable should they suddenly stand following vigorous exercise

40
Q

Fainting or Syncope

Emotional Stress

A

Stress or fright

•

•Reflex dilation of blood vessels

•

•Pooling of blood in the extremities

41
Q

Fainting or Syncope

Cardiac origin

A

•Transient decrease in cardiac output as a result of severe bradycardia or tachycardia

•

•Diminishes cardiac output

•

•Usually sudden onset which resolves when arrhythmia settles

42
Q

Fainting or Syncope

Clinical signs and symptoms

A
  • Slow pulse initially (increases as recovery occurs)
  • •Cold and clammy skin
  • Pale colour
  • Pupils equally dilated
  • •Shallow to normal breathing
  • •Reduced level of consciousness
43
Q

Fainting or Syncope

Management

A

•Maintain in recumbent position (facilitates cerebral perfusion)

•

•Ensure open airway

•

•Loosen tight or restrictive clothing

•

  • Elevate lower limbs (facilitates venous return)
  • Initiate secondary survey and treat any injuries caused by the fall

•

•Encourage patients to remain in recumbent position until fully recovered

•

•Monitor for any change in condition

Technician Course MOD D 2016 (27 decks)

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