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Semester 2 Case Studies > Case 9 > Flashcards

Case 9 Flashcards

1
Q

what is shock

A

a condition associated with circulatory collapse, when the arterial BP is too low to maintain adequate supply of blood to the tissues

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2
Q

what are the signs of shock

A
  • cold, sweaty skin (hypovolemic shock)
  • warm, flushed skin (septic shock)
  • weak and rapid pulse
  • irregular breathing
  • decreased level of consciousness
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3
Q

reasons for shock

A
  1. decrease in volume of blood (hypovolemic shock)
  2. circulatory shock and Haemorrhagic shock fall under category of hypovolemic shock
  3. by reduced activity of the heart (cardiogenic shock) as in MI and PE
  4. Due to widespread dilation of blood vessels so there is insufficient blood to fill them. result of severe septic shock
  5. by a severe allergic reaction (anaphylactic shock)
  6. emotional shock due to a personal tragedy or as a result to the spinal cord
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4
Q

what is shock characterised by

A

systemic hypotension as a result of reduced cardiac output or because of reduced effective circulation blood volume

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5
Q

what are the three stages of shock

A
  1. a non-progressive stage
  2. a progressive stage
  3. an irreversible stage
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6
Q

what is the non progressive stage of shock

A
  • normal circulatory compensatory mechanisms eventually cause full recovery without help.
  • neurohumoral mechanisms help to maintain cardiac output and blood pressure which results in tachycardia, peripheral vasoconstriction
  • cutaneous vasoconstriction is responsible for patients coolness and pallor of skin
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7
Q

what is the progressive stage of shock

A

without therapy the shock worsens until death
- widespread tissue hypoxia, resulting in anaerobic glycolysis and subsequent build up of lactic acid
-
this leads to ‘metabolic acidosis’ which causes dilation of the articles and subsequent pooling of blood in the microcirculation
- widespread tissue hypoxia eventually leads to organ failure

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8
Q

what is the irreversible stage of shock

A
  • the shock has progressed to an extent where therapy is inadequate to save the person’s life
  • lysosomal enzyme leakage results in widespread cell injury
  • nitric oxide released worsens myocardial contractile function
  • schema of the bowel may cause intestinal flora to enter circulation and cause septic shock
  • at this stage the patient has complete renal shutdown and this leads to death
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9
Q

what exacerbates the state of shock

A

electrolyte disturbances and metabolic acidosis

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10
Q

diagram from inadequate perfusion to cell death

A
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11
Q

what is hypovolemia

A

diminished blood volume

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12
Q

what is the most common type of shock

A

hypovolemic shock

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13
Q

what is hypovolemic shock caused by

A

insufficient circulating blood volume - haemorrhage

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14
Q

how does haemorrhage affect the cardiac output

A

haemorrhage decreased the filling pressure of the circulation and as a consequence, decreases the venous return.
as a result the cardiac output decreases

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15
Q

what does the decrease in arterial pressure do

A

simulates sympathetic reflexes that result in:

  • arteriole constriction - increase total peripheral resistance
  • venous contraction - increases systemic filling pressure
  • increase in heart activity
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16
Q

what are sympathetic reflexes essential for

A

survival during blood loss

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17
Q

relationship between sympathetic reflexes, arterial pressure and cardiac output

A

the sympathetic relaxes maintain the arterial pressure at a higher level for longer tha. the cardiac output.
the arterial pressure in minted by increasing th TPR which has no effect on the cardiac output
the venous contstrition prevents the decrease in venous return and cardiac output from falling too low by still maintaining arterial pressure

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18
Q

what does the plateau in the graph a result go

A

central nervous system ischaemic respone, this provides extreme stimulation of the sympathetic nervous system

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19
Q

what happens to the coronary and cerebral circulatory systems

A

they dont undergo vasoconstriction

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20
Q

progressive shock

A
  • exceeding the critical threshold causes shock to become progressive and can lead to death
  • the shock itself causes more shock and turns into a vicious circle that eventually leads to deterioration of the circulation
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21
Q

what is non-progressive shock

A

shock that is not severe enough to cause its own progression

therefore shock of this degree is called non-progressive shock, meaning that the sympathetic reflexes and other factors (humeral) compensate enough to prevent further deterioration of the circulation

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22
Q

what is circulatory shock

A

inadequate blood flow thought the body and reduced cardiac output

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23
Q

what two factors can severely reduce the cardiac output

A
  1. abnormalities that decrease the ability of the heart to pump blood
  2. factors that decrease venous return
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24
Q

what can the CO be normal yet the person is in circulatory shock

A

this can be a result of excessive metabolic rate and abnormal tissue perfusion patterns, so most of the cardiac output is passing through the blood vessels besides those that supply the local tissues with nutrition

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25
Q

what is cardiac depression

A

fall in arterial pressure causing a decrease in the coronary blood flow to the myocardium. this weakens the heart muscle and therefore decreases the CO more.

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26
Q

what does CD create

A

a positive feedback cycle whereby the shock becomes more and more severe

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27
Q

what is vasomotor failure

A

initially the sympathetic reflexes help maintain CO and arterial pressure.

eventually diminished blood flow to the brains vasomotor centre depresses it so much that it too becomes progressively less active and finally totally inactive

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28
Q

what is acidosis a result of

A

anaerobic tissue metabolism continuing without tissue blood flow to remove the acidic by products (lactate)

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29
Q

how is cardiac depression cause by endotoxin

A

endotoxin is released from the bodies of dead gram-negative bacteria in the intestines

diminished blood flow to the intestines causes enhanced formation and absorption od endotoxin

the circulatory toxin the causes increased cellular metabolism despite inadequate nutrition of the cells

this causes cardiac depression

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30
Q

generalised cellular deterioration and cardiac depression diagram

A
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31
Q

what are heart blocked that occur below the AV node called

A

infra-Hisian blocks

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32
Q

what are heart blocks that occur within the fascicles of the left bundle branch known as

A

hemlocks

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33
Q

what is a right bundle branch block

A

this is a defect in the hearts electrical conduction system

during a right bundle branch block the right ventricle is not directly activated by impulses travelling through the right bundle branch

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34
Q

what happens to the left ventricle during a RBBB

A

still normally activated by the left bundle brach

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35
Q

what does the left bundle branch do in RBBB

A

the impulses are able to travel through the myocardium of the left ventricle to the right ventricle and depolarise the heart this way

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36
Q

describe characterises of ECG of RBBB

A

as conduction through the myocardium is slower that conduction through the bundle of His, the QRS complicit is widened

  • deep S waves in leads 1 and V6
  • tall late R wave in lead V1
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37
Q

ECG of RBBB

A
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38
Q

Description of LBBB

A

There is late activation of the left ventricle which causes it to contract later than the right ventricle

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39
Q

LBBB on an ECG

A
  • deep S wave in lead V1

- tall late R wave in leads 1 and V6

40
Q

what is a bifascular block

A
  • conduction abnormality in the heart where two or more of the three main fascicles of the bundle of his are blocked
41
Q

what are the three main fascicles

A
  1. right bundle branch
  2. left anterior fascicle
  3. left posterior fascicle

block of the remaining fascicle will result in complete AV block

42
Q

what can LBBB be causes by

A

aortic stenosis, acute MI,extensive CAD

43
Q

what is compartment syndrome

A

a painful condition in which the circulation and function of tissues are compromised by an increased pressure in the fascia that encapsulates the tissues

44
Q

what is compartment syndrome cause by

A

bleeding or swelling within an enclosed bundle of fibres

45
Q

what is a compartment

A

the space within the fascia

46
Q

what is fascia mostly composed of

A

collagen. the tough fascia keeps the tissues in place and does not easily expand or stretch so the pressure inside the compartment can increase if bleeding or swelling occurs

47
Q

what is a major adverse outcome of compartment syndrome

A

ischaemia

48
Q

what are the three theories that explain the development of tissue ischaemia

A
  1. the increases compartmental pressure may lead to arterial spasm
  2. the critical closing pressure theory
    - CCP is the internal pressure at which a blood vessel collapses and closes completely
    - if the arteriolar blood pressure falls below the crucial closing pressure then the vessel collapse
    - if tissue pressure increase about the Cap
  3. if tissue pressure rises then veins will collapse due to thin walls. if blood continues to flow from the capillaries the venous pressure will rise until it exceeds tissue pressure. this leads to an increase in venous pressure and therefore reduces the arteriovenous gradient and as a result reduces tissue blood flow
49
Q

what is released when the muscles become hypoxic

A

histamine like substances are released causing vasodilation of the capillary bed and increasing endothelial permeability

50
Q

what are the common causes of compartment syndrome

A

tibial or forearm fractures, prolonged limb compression, crash injures and burns

51
Q

compartment syndrome flow diagram

A
52
Q

how is pulmonary artery pressure ,measured

A

by inserting a catheter

53
Q

what is the name of the catheter inserted into the pulmonary artery

A

the Swan-Ganz catheter

54
Q

what does the PA catheter detects

A
  • detect heart failure
  • monitor therapy
  • evaluate effects of drugs
55
Q

what pressures can the Swan-Ganz catheter measure

A
  • right atrium
  • right ventricle
  • pulmonary artery
  • left atrium filling pressure
56
Q

what is the procedure of the SGC

A

the catheter is introduced through a large vein - internal jugular, subclavian or femoral

it is then threaded through the right atrium, the right ventricle and into the pulmonary artery

a chest X-ray should always be obtained to check the final position of the catheter

57
Q

the Swan-Ganz catheter description:

A
  • the catheter has two lumens and is equipped with an inflatable balloon at the tip, which facilitates its placement into the PA through the blood flow
  • the balloon when inflated causes the catheter to wedge in a small pulmonary blood vessel
  • the catheter is wedged so that it can provide an indirect measurement of the pressure in the left atrium

it is monitored and guided by the pressure waveforms recorded from the viral

58
Q

what does fluid replacement therapy involve the administration of

A
  • crystalloid

- colloid

59
Q

example of a crystalloid

A

NACL- also known as saline

60
Q

what does saline do to the blood

A

adds volume as well as electrolytes

61
Q

example of colloid

A

gelofusine

62
Q

what do colloids do

A

they are volume expanders that are used as blood plasma replacement if a significant amount of blood has been lost

it causes an increase in the BV, blood flow, cardiac output and oxygen transportation

colloids are big molecules so when they are adminitisteredt they draw in extracellular fluid into the blood as a result of osmosis

63
Q

what does mechanical ventilation rely on

A

generating postive presser

64
Q

what does the ventilating pump do

A

forces in air into the lungs and then allow the elastic recoil to carry out expiration

65
Q

what are complications of artificial ventilation

A
  • life threatening effects of loss of airway
  • barotrauma - tension pneumothorax
  • impaired cardiac function due to compression of the heart
  • inappropriate ventilation for patient needs
66
Q

what is diamorphine

A

heroin

67
Q

what is heroin

A

narcotic analgesic - pain killer

68
Q

mechanism of action of diamorphine

A
  • it is a mu-opiod agonist
  • it acts on endogenous mu-opiod receptors in the brain
  • diamorphine is then converted into morphine before crossing the blood brain barrier and agonising the mu-opiod receptors
  • however, taken IV, the diamorphine itself crosses the blood brain barrier. it is rapidly metabolised into morphine once in the brain
  • morphone then agonises the opiod receptors
  • endorphins are released in the brain and nerves, attenuating pain
69
Q

what is unconsciousness

A

mental state that involves complete or near-complete lack of responsiveness to people and other environmental stimuli

70
Q

what is the neurological scale that measure the level of consciousness

A

Glasgow Coma Scale

71
Q

how is the patient assessed using the GCS

A

the patient is assessed against the criteria and the resulting points give a patient a score between 3 (deep unconsciousness) and either 14(original scale) or 15(modified scale)

72
Q

what is the E element of the GCS scale

A

eye response

4 - spontaneous
3 - to voice
2- to pain
1- none

73
Q

what is the V element of the GCS scale

A

verbal responses

5- normal conversation 
4- disorientated conversation 
3- words but non coherent 
2- no words 
1- only sounds
74
Q

what is the M element of the GCS scale

A

Motor response

6- normal 
5- localised to pain 
4- withdraws to pain 
3- abnormal posture 
2- abnormal posture 
1- none
75
Q

can you score less than three

A

no

76
Q

classification of brain injury

A 
severe = 3-8 
moderate = 9-12 
mild = 13-15
77
Q

what three conditions need to be met for agreement of treatment to be legally acceptable

A

consent must be informed to an adequate standard

patients must be competent to consent to treatment

patients must not be conserved into accepting treatment against their wishes

78
Q

when can treatment be given to adult patients without consent

A

if they are temporarily or permanently incompetent to provide it and they havent previously refused such future treatment in a legal way with the legal aurthority to do so

further, given the condition of such patients, treatment must be necessary to save a life or prevent permanent injury.

79
Q

how can clinicians breach their professional duty to obtain adequate consent

A

through not providing a reasonable amount of information about the risks of proposed treatment

80
Q

Henderson hasselbalch equation diagram for acid base questions

A
81
Q

what is located in the carotid sheath

A

the vagus nerve is in the middle of two large vessels: the common carotid artery and the internal jugular vein which makes up the carotid sheath

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82
Q

NICE guidelines on fluid after trauma pre hospital

A

fluid should only be given if a pulse cannot be found.

250mls of fluid should be given at a time and after the pulse should be felt for and if pulse still cannot be found give another dose of fluids

crystalloid fluids should be given pre hospital

83
Q

what is a urinary catheter called

A

Foley catheter

84
Q

how is a urinary catheter used

A

The catheter is held in the bladder by a water-filled balloon, which prevents it falling out. These types of catheters are often referred to as Foley catheters. Urine is drained through a tube connected to a collection bag, which can either be strapped to the inside of your leg or attached to a stand on the floor.

85
Q

why is a urinary catheter used

A

to measure the urine output of critically ill people

86
Q

what is the normal urine output

A

urine output is 1-2 ml/kg/hr. To determine the urine output of your patient, you need to know their weight, the amount of urine produced, and the amount of time it took them to produce that urine. Urine output should be measured at least every four hours if possible

87
Q

why is diamorphine faster acting than morphine

A

as it goes directly to the brain and is turned into morphine after it crosses the blood brain barrier

88
Q

how does diamorphine block pain

A

Diamorphine mimics the action of endorphins by combining with the opioid receptors in the brain and spinal cord. This blocks the transmission of pain signals sent by the nerves to the brain. Therefore, even though the cause of the pain may remain, less pain is actually felt.

89
Q

mode of action of tranexamic acid

A

Tranexamic acid is a synthetic derivative of the amino acid lysine and binds the 5 lysine binding sites on plasminogen. This inhibits plasmin formation and displaces plasminogen from the fibrin surface. It may also directly inhibit plasmin and partially inhibit fibrinogenolysis at higher concentrations.

Tranexamic acid competitively and reversibly inhibits the activation of plasminogen via binding at several distinct sites, including four or five low-affinity sites and one high-affinity site, the latter of which is involved in its binding to fibrin. The binding of plasminogen to fibrin induces fibrinolysis - by occupying the necessary binding sites tranexamic acid prevents this dissolution of fibrin, thereby stabilizing the clot and preventing hemorrhage.5

90
Q

how does ICU affect mental health

A

Critically ill patients may develop problems with falling or staying asleep. They may have nightmares and unwanted memories. Reminders of their illness may produce intense feelings or strong, clear images in their mind. Their reactions to these feelings may be physical or emotional.

Patients may also feel depressed and anxious and may have symptoms of posttraumatic stress disorder (PTSD). These include having nightmares and unwanted memories, feeling “keyed up,” and wanting to avoid thinking or talking about their stay in the ICU.

91
Q

the AVPU scale

A

A - the patient is awake
V - the patient responds to verbal stimulation
P - the patient response to painful stimulation
U - the patient is completely unresponsive

92
Q

what are the different types of mechanical and artificial ventilation

A

The two main types of mechanical ventilation include positive pressure ventilation where air is pushed into the lungs through the airways, and negative pressure ventilation where air is pulled into the lungs.

93
Q

what is negative pressure ventilation

A

Iron lung: The first mechanical ventilator, a metal cylinder which enveloped the patient completely up to the neck.
Chest cuirass: A small shell which can be strapped to the patient’s chest to create the negative pressure.

94
Q

what is positive pressure ventilation

A

Positive-pressure ventilators were developed in the early 1950s to treat polio patients with respiratory paralysis. These ventilators blow the air into the patient’s lungs through a tube. They may be invasive or noninvasive.

95
Q

what is invasive ventilation

A

Endotracheal intubation: the tube is inserted into the patient’s airway (trachea) through the mouth or nose.
Tracheostomy: the tube is inserted through a hole made into the airway.

96
Q

what is non invasive ventilation

A

Continuous positive airway pressure (CPAP): delivers constant and steady air pressure.
Autotitrating (adjustable) positive airway pressure (APAP): changes air pressure according to the breathing pattern.
Bilevel positive airway pressure (BiPAP): delivers air with different pressures for inhalation and exhalation.

97
Q

how does positive pressure ventilation work

A

Currently positive pressure ventilation is the common form of mechanical ventilation in hospitals. The positive-pressure ventilators push the air into the patient’s airway. The ventilator continually blows and stops in regular preset cycles enabling the lungs to receive oxygen and expel carbon dioxide. Positive-pressure ventilators may be

Volume-controlled: delivers a preset volume of air into the patient’s trachea even if it entails high airway pressure. When the flow is stopped the chest recoils and expels the air out.
Pressure-controlled: delivers air till the airway pressure limit is reached and the valve opens to expel air. The volume of air delivered may vary depending on the airway resistance and lung capacity.
Dual control: these combine the advantages of volume control and pressure control and deliver airflow based on the requirement and response of the patient.

Semester 2 Case Studies (11 decks)

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