OLT test study Flashcards

1
Q

structures of the circulatory system

A

 The heart (pump)
- Right side to pulmonary circulation
- Left side to systemic circulation
 Peripheral vascular system (tubing)
- Arteries carry oxygenated blood (except for pulmonary arteries)
- Veins carry de-0xygenated blood (except for Pulmonary and umbilical veins)
 Hematological system (blood and components)
- Closely inter-linked with the lymphatic system

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2
Q

function of circulatory system

A

 Deliver oxygen, nutrients and other requirements to the cells
 Remove and transport waste, such as carbon dioxide to be excreted
 Your heart pumps ~ 80 bpm/minute x 80 yrs = 3,363,840,000 times in a lifespan!!!

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3
Q

blood pathway

A

Blood from right atrium enters right ventricle and pulmonary arteries carry deoxygenated blood from right ventricle to lungs for oxygenation. Two pulmonary veins come from each lung and pass O2-rich blood to left atrium. Blood enters left ventricle from the left atrium.

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4
Q

arterial blood supply originates?

A

aorta

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5
Q

coronary arteries originate

A

originate at the start of the aorta to feed the myocardium and they form venules that become veins that empty into the right atrium itself via the coronary sinus

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6
Q

main influence of coronary circulation

A

the pressure in the Aorta of itself (basically from left ventricle pressure).

  • Several disorders of the heart affect heart contraction, therefore strength of the blood being pumped out therefore affecting the strength of the blood being pumped out and therefore the flow of blood of the into heart itself and into the system
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7
Q

blockage or spasm of partcular coronary aretery can leadto…

A

ischemia of that part of the myocardium fed by that blood vessel.
- The type of myocardial infarction depends on what coronary artery/ branch of an artery is blocked or spasming…

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8
Q

examples of coronary arteries

A
right coronary artery
marginal artery
posterior interventricular artery
anterior decending artery
circumflex artery
left coronary arteru
aorta
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9
Q

examples of coronary veins

A
superior vena cava
anterior cardiac veins
small cardiac vein
middle cardiac vein
coronary sinus
great cardiac vein
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10
Q

what is the pericardial sac

A
  • surrounds the heart. protects cushions and anchors it in place with his various blood vessels and surrounding structures
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11
Q

structures of the heart wall

A

three layers of the pericardium down through the three linings of the heart wall itself.

	Pericardium
Parietal and visceral
Pericardial cavity and fluid
	Myocardium
	Endocardium
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12
Q

functions of the pericardium (outermost layer)

A

protection, its receptors that respond to changes in blood pressure and pulse at the relative thickness of the myocardium which is much thicker

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13
Q

t or f

continuous supply of blood is essential to body function

A

t

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14
Q

what facillitates one way blood flow

A

Correct functioning heart valves facilliitate the one way blood flow, opening and closing of valves functioning correctly

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15
Q

valves during diastole

A

Diastole (ventricles filling)- the 2 AV valves are open, SL valves closed

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16
Q

what happens to valves once ventricles are full?

A

When ventricles are full AV valves close, SL valves open

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17
Q

what are the valves

A
	Atrioventricular valves
- Tricuspid valve
- Mitral valve
	Semilunar valves
- Pulmonary semilunar valve
- Aortic semilunar valve
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18
Q

what is cardiac action potential

A

transmission of electrical impulses that form the conduction system that coordinated the rhythmical nature of the heart

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19
Q

where is AP initiated in heart

A

AP is initiated in Nodes (Specialized cells that generate and transmit without any nervous system initiation)

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20
Q

what is invlolved in the hearts conduction system

A
	Sinoatrial node (SA)- pacemaker of the heart
- Intranodal pathways
	Atrioventricular node (AV)
	Bundle of His (AV bundle)
	Right and left bundle branches
	Purkinje fibres
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21
Q

what is preload

A

 Preload (the initial stretching of the cardiac muscle cells prior to contraction)

  • Left ventricular end-diastolic volume
  • Frank-Starling law of the heart
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22
Q

What is afterload

A

 Afterload ( the force or pressure against which the heart has to contract to eject the blood).
- Resistance that must be overcome for blood to be ejected

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23
Q

what is contractility

A

 Contractility (Sstrength and vigour of the heart’s contraction during systole)

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24
Q

What is stroke volume

A

 Stroke volume ( The amount of blood pumped by the left ventricle of the heart in one contraction.)

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25
Q

what is ejection fraction

A

 Ejection fraction ( is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction)

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26
Q

how many sections of the respiratory system

A

Divided into upper and lower but does function as a whole

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27
Q

upper respiratory system is composed of ?

A
  • The nose (filters the air, mucus trapping dust and bacteria which is then destroyed by enzymes, air is also warmed by excellent blood supply)
  • Sinuses ( several, hollows in the skull that make it lighter)
  • Pharynx ( tube in 3 parts that extends from the back of the nose to the larynx that is the path of food and air)
  • Larynx ( 5 sm, shorter, contains vocal cords and voice box, at entrance there is the epiglottis which only allows air to enter)
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28
Q

mucus combined with cilli in upper resp work to?

A

The mucus combined with cilia work to move the foreign debris by either cough/ spitting out (expectorating) or swallowing

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29
Q

why do we need defence mechanism in upper respiratory system

A

because we have a dirty environment in our upper respiratory.
Mouth< is bacteria contaminated
Lower airway< is sterile When functioning well the airway becomes cleaner the further you go down.

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30
Q

structires of uppr airway (conducting zone)

A

• Conducting airways

Upper airways
•	Nasopharynx
•	Oropharynx
•	Larynx
•	Connects upper and lower airways
Lower airways
•	Trachea
•	Left and right bronchus
•	Secondary bronchi
•	Tertiary bronchi
•	Bronchioles
•	Terminal bronchioles
•	Respiratory bronchioles
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31
Q

3 stages of respiration

A

Respiration has three stages:

  1. Ventilation
  2. Diffusion
  3. Perfusion
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32
Q

main function of upper respiratory

A

conducts air especially oxygen.

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33
Q

why is there often inflammation in upper airways

A

Upper airway is designed to remove foreign debris including microorganism meaning the upper respiratory system is constantly exposed to potential infections and inflammatory conditions.

You will see this In: children< as they develop their immune system
Older adults< as their immune system begins to weakened.
URTI< Upper respiratory tract infection

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34
Q

descrive viral URTIs

A

• Most common
• Highly contagious
Droplet, direct contact
Contact forms immunity but many types…
• Commonly are rhinoviruses and RSVs (Respiratory syncytial virus)
• But there are many other viruses
Adeno/parainfluenza/respiratory syncytial +++
• Symptoms form from inflammatory response
Swollen mucous membranes
Nasal congestion and secretions
Headache, fever, general malaise (which is A general sense of being unwell often accompanied by fatigue, diffuse pain or lack of interest in activities.)

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35
Q

describe the influenza

A

• Highly contagious, many subtypes, type A most common
• Respiratory and systemic symptoms (With severity of symptoms usually worse than common cold >muscle weakness, general malaise and more severe fever)
• There is a greater chance of a flu proceeding to form pneumonia, sinusitis and middle ear infection.
• Older adults are at risk of bacterial infections due to debilitated condition. This can occur due to their condition.
• Most people treat themselves often over the counter treatments> cold and flu decongestants tablets, analgesic and histamine.
• It is a virus not a bacterial infection, so antibiotics are unnecessary. Sometimes they are prescribed to those at risk e.g. To patients who are very old to prevent bacterial infection coming in on top of the virus.
>Plenty of rest and fluid needs to encourage.

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36
Q

describe flu vaccine

A

• Encourage vaccinations
Influenza has three types of flu viruses: Type A, B and C
Type A and B have up to 20% of population sniffling, aching, coughing and running high fevers.
Type C causes flu, however, the symptoms are much less severe

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37
Q

descibe sinitis

A
  • Bacterial or viral (or fungal), acute or chronic
  • Develops when sinuses blocked, swell, inflame and pressure
  • Greater risk in older adult or immuno-compromised
  • Treatment varies
  • Restore drainage
  • Treat infection
  • Relieve symptoms
  • Irrigation/surgery
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38
Q

development of sinitis

A

( Bacterial or viral infections can travel up to the nose causing swelling, congestion and blocking of the opening leading to great pressure, swelling and inflammation > Increase headaches and feeling of general malaise

Nasal polyps or other types of nasal obstruction can increase the risk of developing sinusitis. As this can affect the pre draining component of the siunus

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39
Q

descrbe Pharyngitis (viral)/tonsillitis (usually bacterial but can be viral)

A

Pharyngitis is often viral but can be bacterial. Often the virus is rhinovirus though in teenage group It can be from the Epstein Bar virus (called kissing disease. Its nickname is ‘mono’).
Pharyngitis and tonsillitis may occur in combination because tonsil as a lymph node seats in the recess in the pharynx.
• Droplet spread
• Pharyngitis
• Symptoms vary, minor or major
• Complications
• Tonsillitis
• Inflamed/painful/fever/lymphadenopathy/general malaise
• Abscess/quinsy
Quinsy can be quite dangerous because it’s a type of abscess that forms in between tonsil and the pharynx > It can increase in size and can block part of the airway.

• If strep. glomerulonephritis (cause of major kidney disease)/rheumatic fever
Pharyngitis symptoms may vary it can go from minor to major e.g. from simple throat to difficulty swallowing.
Tonsillitis symptoms may vary from minor to major. Tonsil are inflamed and painful> increasing fever, increase size of a lymph node (lymphadenopathy) and general malaise abscess or quinsy.

  • Correct diagnosis (Whether its viral and bacterial. Then adjust the treatment accordingly)
  • Treatment
  • Antipyretics/analgesia/symptomatic/antibiotics
  • Tonsillectomy - If the patient suffers from regular dosage of tonsillitis

Antipyretics< to get the temperature down
Analgesic< to relieve pain
Symptomatic treatment< if it is bacterial you give antibiotics
If the patient suffers from regular dosage of tonsillitis.

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40
Q

describe epiglottitis

A

Epiglottis< Its viral. Its uncommon but when it does occur it is an emergency > Obstruction in the airway, laryngospasm (temporarily difficult to speak or breathe
• Uncommon but an emergency
• Obstruction, laryngospasm
• Antibiotics, steroids, close monitoring
• Laryngitis
• Usually viral
swollen, oedematous vocal cords (Result in hoarse voice or loss of voice all together.)
• Conjunction with other respiratory conditions
• Rest, fluids

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41
Q

describe laryngitis

A
  • Usually viral
  • swollen, oedematous vocal cords
  • Conjunction with other respiratory conditions
  • Rest, fluids maybe with with analgesic
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42
Q

describe pertussis

A

Pertussis is a whooping cough
• Highly contagious bacterial infection
• Droplet spread
• Life threatening in infants, less so as older
• Complications
• Hypoxic brain injury, pneumonia
• The bacteria/toxins
• Cause inflammation, inhibits immune responses, affect cilia…
…Foreign material/ microorganism that are usually remove by natural processes stay in the lungs, in the airway and develop other infection such as pneumonia.

Pertussis starts off with classic flu> Rhinovirus symptoms (nasal dryness, irritation, sore throat/ throat irritation, nasal discharge, nasal congestion and sneezing, headache, facial and ear pressure, loss of sense of smell and taste)
And builds up to a week later with coughing> gradually increases intensity to> Paroxysmal coughing.
• Classic ‘flu symptoms paroxysmal coughing
• Treatment – antibiotics (usually erythromycin), hospitalisation

Best protection is vaccination. * highly recommended for pregnant women because it protects the newborn.

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43
Q

describe epitaxis/ nasal trauma

A

Epistaxis/ nasal trauma often caused by trauma/ punched on the nose/ nose picking/ cocaine abuse.
• Major arterial supply ( Nose has major arterial supply. When it bleeds it bleeds heavily. )
• Trauma, cocaine abuse
• Underlying health disorder
• Treatment
• Pinch nose, head forward, ice (Head forward so blood doesn’t run into the stomach because it can cause nausea and vomiting. It also cannot be measured)
• Topic vasoconstrictors
• Cauterisation (chemical, diathermy)
• Nasal packing (anterior and posterior)
Nasal packing is basically a nasal tampon. Children have anterior bleed and posterior bleed is more likely for adults. Or you can have both.

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44
Q

lower respiratory syetem comprised of

A
  • The bronchi
  • The lungs
  • The alveoli
  • The pleura
  • The ribs
  • Intercostal muscles.
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45
Q

what is the respiratory zone

A

Respiratory zone< where gas exchange diffusion, perfusion occurs.
Most bronchioles and large airways are part of the conducting zone of the lung, which delivers gas to sites of gas exchange.

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46
Q

what is ventilation and perfusion

A

Ventilation< refers to the flow of air and out of the alveoli.
Perfusion< refers to flow of blood to alveolar capillaries.

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47
Q

what is the carina

A

The trachea at the carina is where it divides into two main bronchi> left and right lung at the level of the sternum.

Carina contains various sensitive nerve ending, this helps with expulsion of dust and foreign particles.

^This part of the airway is known to go for Bronchospasm if over stimulated. This occur from a result of several disease processes including asthma/ number of different medication/ anaphylactic.

Endotracheal tube< can result in life threatening hypoxia.
Bronchi branches> have thinner walls
Bronchioles (looks like a tree)> Very thin membrane around them to allow gas exchange diffusion to occur
Trachea > Thick walls

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48
Q

what are the gas exchange airways

A
•	Respiratory bronchioles (With a membrane consisting one cell around them)
Bronchioles> terminates in the alveolar ducts that contains the alveoli
•	Alveolar ducts
•	Alveoli 
•	Epithelial cells (pneumocytes)
•	Squamous type I alveolar cells
•	Covers 95% of alveolus surface area
•	Rapid gas exchange
•	Great type II alveolar cells
•	Surfactant production
•	 Covers 5% of alveolus surface
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49
Q

what is paranchyma

A

Parenchyma means functional part> parenchyma of liver/lungs/kidney and all functional part of those organs

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50
Q

what is involved in the pulmonary ciruculation

A
  • Right side of heart
  • Pulmonary artery
  • Pulmonary capillaries
  • Pulmonary vein.
  • Alveolar-capillary membrane
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51
Q

wall of smallest alveoli are how thick

A

one cell thick

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52
Q

Describe third process of respiration

A

The third process of respiration- perfusion. Provides the blood to off low CO2 and pick up O2 oxygen. Provide nutrients to the pulmonary tissues and provide filter system as blood enters from right ventricle.

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53
Q

what does the pulmonary artery do

A

Pulmonary artery< Deoxygenated blood from heart to lungs (the only artery that carries deoxygenated blood in the body)

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54
Q

is the pulmonay system low pressure

A

Pulmonary system is low pressure system meaning the right ventricle in normal circumstance doesn’t have to pump as hard as left ventricle, which pumps oxygenated blood out against resistance into the system of the body.

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55
Q

what happens at the alveolar capillary membrane

A

Alveolar capillary membrane is where blood and air goes through across very thin membrane.

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56
Q

what is cerebral blood flow

A

The brain receives a constant supply of blood, which is essential for normal brain functioning.

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57
Q

what is cerebral blood volume

A

amount of blood in the cranial vault (approx 10% of total intracranial volume- CSF and brain tissue make up remainder)

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58
Q

t or f brain hs high metabolic activity

A

 Brain has high metabolic activity however is not able to perform anaerobic metabolism and requires continual supply of o2 and glucose

 Brain not able to store ATP and glycogen which are essential for metabolism ( therefore if there is even a short interruption to blood supply it can have devastating effects

 Brain is able to maintain cerebral blood flow despite changes in peripheral blood flow (exact mechanism is unknown but because of this it is able to ensure the brain received the oxygen and glucose it requires for maintaining normal brain activity.

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59
Q

describe cerebral circulation

A
  • brain receives approx. 15-20% of cardiac output
  • Cerebral circulation is designed to ensure if a vessel is blood there is an alternate vessel
  • (collateral circulation)
     Circle of Willis – series of interconmected vessels that ensure blood supply to the brain. Fed by 2 internal carotid arteries and 2 vertebral arteries. if blood flow ceases for even a few minutes an individual will become unconscious.
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60
Q

what is the monroe kellie doctrine

A

The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis

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61
Q

describe the components of the monroe kellie doctrine

A

 The brain, blood and CSF are situated in a rigid vault.
Blood 10%
CSF – 10%
Brain Tissue – 80%
 Sum of volumes of brain, CSF, and intracranial blood is constant- no room for expansion in cranial vault.
 An increase in one should cause a decrease in one or both of the remaining two as a normal compensatory mechanism:
Increase blood = reduced CSF to compensate
Increase in brain mass = reduced blood and CSF to compensate
Increased CSF = reduced blood to compensate

62
Q

what is normal intracranial pressure

A

 Normally 5-15mmHg
 Measured by placing a catheter into the lateral ventricle
 Place catheter into lateral ventricles, catheter is connected to transducer which turns pressure into wave form
 ICP is approx. equivalent to pressure of CSF
 Represents sum of pressure exerted by 3 components of csf

63
Q

what does knowing ICP allow us to do

A

 Icp helps provide info to guide intervention and prevent secondary cerebral ischemia and brainstem distortion and herniation
 Icp monitoring not generally indicated for patients with mild brain injury (GCS of 9-15) but may be appropriate for comatose patients or patients with severe brain injury (GCS 3-8)

64
Q

what caiuses increased ICP

A

 Caused by an increase in intracranial content
 Tumour growth, oedema, excessive CSF or haemorrhage
 Initially asymptomatic due to compensation
 As compensation fails compromises oxygenation and neurological function
 With increased pressure brain is no longer able to compensate, body attempts to overcome by vasoconstriction elevating bp and pushing o2 into cranial space
 Hypoxia and hypercapnia [atients condition deteriorates rapidly
 Unconsciousness-> progressively deeper coma
 Breathing from normal to rapid and abnormally deep ( central neurogenic hypoventilation)
 Pupil changes- small and reactive to ipsilateral dilation (dilation on same side of injury or pressure on ocular motor0 through fixed to bilateral dilation
 Widening pulse pressure
 Bradycardia

65
Q

what is cushings triad

A
  • 3 classic signs of ICP
    increased pulse pressure, irregular breathing, decreased pulse
  • If prolonged brain damaged and non reversable
  • Syndrome usually in late stage of brain herniation
66
Q

what is herniation

A
  • ICP not uniform across brain compartments
  • Brain tissue can shift from areas of high pressure to compartments of low pressure, this is called herniation.
  • There are a number of different routes which brain tissue can herniate depending on the sight of injury
67
Q

types of cerebral herniation

A

 Classified in area where occurring, most common are uncal and central herniation

 Cingulate Herniation – cingulate gyrus compressed under falx cerebri

 Central Herniation - downward displacement of brain structures – cerebral hemisphere, basal ganglis, midbrain.. see loss of consciousness that progresses to coma, Cheyne strokes breathing patterns and pupils that progress to midsized and fized.
((tonsillar herniation)– cerelellar tonsils through the foramen magnum, compressing brainstem)

 Uncal or Lateral Herniation – lateral mass displaces cerebral tissue centrally, herniation of the medial temporal lobes through the tentorium into brainstem, see in ipsilateral pupil dilation on side of trapped ocular motor nerve, see loss of consciousness, motor deficiets, decress sensation, resp changes

 Infratentorial Herniation – increased pressure in infratentorial compartment. Herniation may be upwards or downwards (compresses medulla- centers for vital functions- see coma, resp alt, fixed pupils, eventual resp/ cardiac arrest.

68
Q

what is cerebral perfusion pressure

A

Blood pressure gradient across brain, determines if neurons receive blood or not
 Blood pressure in brain is cerebral perfusion pressure (CPP)
 CPP = MAP(Mean Arterial Pressure) – ICP
 Normal range CPP is 70-100mmHg
 Less than 60 in adequate, hypoxia and cell death may occur

69
Q

relationship between CPP and ICP cycle

A

increase in ICP decreased cerebral blood flow decreasing CPP-MAP-ICP whicg decreases blood flow to affected area of the brain causing ischaemia eventually leading to infarction of brain tissue resulting in rswelling that manifests as cerebral odema which then exacebates space occupying lesions, hydrophalus or cerebral haemorrage which contributes to increase ICP

70
Q

what is cerebral odema

A

 Is an increase in fluid content of brain tissue
 Can occur following trauma, infection, haemorrage, ischemia, hypoxia, tumor, infarct
 Not uncommon in neurological illnesses
 Once odema begins progess is rapid and difficult to control
 Causes expansion in brain tissue and can lead to Increased ICP, leading to distortion of blood vessel displacement of brain tissue and eventual herniation
 Seen in patients 24 hours- 48 hr post injury or insult peaking 72 hours after

71
Q

management of increased ICP

A

 Mannitol Administration (hypertonic solution used to decrease cerebral odema- plasma expanding effects reducing viscosity, increases cerebral blood flow and oxygen metabolism causing vessels to decrease in diameter= reduction in cerebral blood volume and ICP while maintain cerebral blood flow)
 CSF drainage
 Respiratory Support (consider avoiding low o2 and over stimulating cogh reflex)
 Analgesics, Sedatives and Paralytics ( to reduce anxiety and diminish awareness of noxious stimuli, suppress coughing and cough reflex)
 Blood Pressure Management ( to ensure effective CPP)
 Seizure Prophylaxis (seizure increases Cerebral metabl rate and cerebral blood flow- treatment to avoid additiona injury)
 Hypothermia (reduce metabolic demean- controversial)
 Decompressive craniectomy (surgical release of skull allowing for expansion of brain tissue0
 Positioning (head and neck neutral position- others can restrict drainage)
 Environmental Considerations (stimuli can increase stress, anxiety, pain making management difficult

72
Q

aim of increased ICP management

A

Aim of treatment is to reduce ICP and maintain adequate perfusion to prevent further injury
Most management orientated to control of cerebral blood flowand csf circulation
Treatment may be initiated when ICP increases above 15mmg of mercury

73
Q

what is consciousness and arousal

A
  • Consciousness – a state of awareness of oneself and the environment and respond to that environment
  • Arousal – individuals state of awareness, mediated by Reticular activation system in brainstem
74
Q

What post coma unresponsiveness and locked in syndrome

A
  • Post Coma Unresponsiveness – complete lack of responses that suggest a cognitive component, preservation of sleep-wake cycles and cardiorespiratory function, partial or complete preservation of hypothalamic and brainstem autonomic functions.
  • Locked in Syndrome – indicates damage to the brainstem without damage to the cerebrum. No abnormality in level of arousal or consciousness.
75
Q

what s mental health/ illness

A

There are no universally agreed definitions of Mental Health or Mental Illness, because there are many variables that can influence definition.
These include:
cultural variables, theortrical views, service delivery modules

76
Q

what are cultural variables

A
  • The way that we perceive mental health and illness as a culture will influence our definition.
  • Depression might be thought of as mental illness in some cultures, and a normal mood state in others.
  • Our collective moral and religious beliefs might influence our interpretation of symptoms and therefore diagnosis.
77
Q

what are theoretrical views

A

Our individual theoretical view might influence our perception:
• A view based on the medical model of diagnosis and treatment
• A holistic view of the whole person within a society, culture, and their wellbeing.
• The lived experience of a service user

78
Q

what are service delivery models

A
  • Severe and enduring illness are commonly treated by mental health teams: therefore this must be mental illness?, but how do we define what’s “severe and enduring”
  • Depression and anxiety are increasingly treated in wellbeing services. Is depression therefore not mental illness, but a normal emotional state?
79
Q

why define mental health

A

Because the way in which we define and diagnose mental illness might influence…
• Our perception of what is normal human emotion and what is a treatable mental illness
For example: we might all say we get depressed at times but wouldn’t all say we’re mentally ill!.

Because our definition of mental illness and individual perception is likely to influence:
•	The structure and funding of services.
•	Mental Health Legislation
•	Treatment models
•	Individual nursing care
80
Q

what is individual perception in mental health

A

So before we attempt to make a definition, it’s important to recognise that we all come to this point with our own idea of what mental illness is. This will might be based on
• Personal Experience
• Our experience of a friend of loved one suffering with an emotional issue
• Our culture
• Our individual beliefs and morals

81
Q

what is mental health literacy

A
  • All nurses require a degree of mental health knowledge, as you will all meet and care for people across all clinical environments, but particularly in:
  • Emergency Departments
  • Maternity
  • Drug and Alcohol services
  • Community and Rural health services
  • Schools

This is knowledge is often referred to as Mental Health Literacy and will include:
• Recognition of cultural diversity
• Customary/traditional knowledge
• Experiential knowledge
• Medical/clinical knowledge
• Social Science knowledge e.g. Social determinants
• Together; this knowledge will help us to understand and care for people with mental illness, across the lifespan, and in all settings.

82
Q

australian perspective of mental health/ illness

A
  • It’s important to recognise that in Australia, mental health provision is still largely based upon the medical model.
  • Within this medical model, nurses provide holistic care across the whole lifespan
  • Services in Australia and most advanced countries are becoming tiered, to reflect current evidence and best practice. This also includes entry point and setting for treatment, which is usually determined by type and severity of illness.
  • A tiered model will depend upon individual community resources but generally look like this..
83
Q

tier one model of mental health care

A
•	Tier 1
Mild conditions: The GP is the care coordinator, other community services also used such as:
Library groups
Men's sheds
Counselors
84
Q

tier 2 model of mental health care

A

• Tier 2
Mild-Moderate conditions
The GP remains the care coordinator prescribing and writing a “mental health care plan”, which will activate Medicare funding for psychological therapy sessions, usually provided by an NGO/NFP (not for profit) provider.

85
Q

tier 3 of mental health care

A

Severe and Enduring mental health conditions: Managed by state-wide mental health services and covering acute, community and rehabilitation services. Key worker will be a member of the mental health team.

86
Q

tier 4 of mental health model of care

A

Forensic and regional secure services.
Smallest amount of service users will be involved in t4.
There is also movement between the 4 tier services, shared care between services but should treat people in right environment with right resources

87
Q

stadardised diagnostic criteria used in australia

A

We use two standardized sets of diagnostic criteria in Australia
• DSM-V: The Diagnostic and Statistical Manual of Mental Disorders (Currently volume 5)
• The DSM-V is currently the benchmark manual used in Australia for the clinical diagnosis of mental illness.
• ICD-10: The International Classification of Diseases, (Section 10: Classification of Mental and Behavioral Disorders)
• The ICD 10 is used in Australia to report and categorize diseases internationally. Often used in research
• The ICD 10 is often referred to by clinicians, but the diagnostic codes are not recorded in clinical practice

  • Diagnosis of mental illness is usually dependent upon the presence of a set of clinical features and symptoms.
  • In Australia, diagnosis is performed by Psychiatrists, and extensively in the case of mild/moderate mental illness by General Practitioners.
88
Q

mental health assessment

A
  • A mental state assessment (MSA) is the standard format used by professionals to assess the status of a persons mental health.
  • It is a tool used by all mental health clinicians
  • Not only mental health professionals use MSA’s, and they are being used increasingly in general settings by general nurses.
89
Q

full mental assessment might include…

A
  • Significant medical history
  • Social circumstances
  • Circumstances of presentation
  • Risk assessment
  • Assessment is fluid and can change rapidly
90
Q

what mental health legislation is there

A

The Mental health Act
All Australian states have their own Mental Health Act.
- Sometimes people with mental illness are unaware that they are ill, (they have no insight to their condition) or their perception of their illness is different to others. We therefore need legislation sometimes in order to assess and treat people when they become acutely unwell, and sometimes long term when their condition is enduring.
- The purpose of mental health law in Australia is not punitive. It is designed to protect individuals suffering from a mental illness and the public, by referring to clinical excellence and least possible restriction on the client.

The Western Australian Mental Health Act 2014
 There is a brand new Mental Health Act currently being rolled out in Western Australia.
 The act is a bold and positive change based on evidence that recognizes the role of the patient, carers and former service users in it’s implementation.
 The new act includes significant changes to the current mental health act tribunal and the role of state funded advocacy services.
 Recognizes that a person’s functioning is subjective, and not merely dependent upon clinical diagnosis and psychiatric opinion.
 Is seen by many as a move away from a predominantly medical model in Western Australia

91
Q

why is there mental health stigma

A

• Stigma is all about negative perceptions of mental illness
• Negative stereotypes of mental ill people are often reinforced in film and other forms of media.
face…(more so than their actual illness!)
• The anxiety of being labeled or treated differently (stigmatisation) and the impact this might have on careers, family and relationships can be significant in a persons recovery.
• Stigma is all about the perception that people with mental health problems are dangerous, or weird, or just plain weak.. The kind of stuff that sells newspapers, movies and other forms of media.
• However.. over 98% of people with a mental illness work and function normally like you and me.

92
Q

stigma as a deterrant in mental health

A
  • Many theorists suggest that certain types of mental illness are largely behavioral and are less likely to be reinforced if the consequences are negative.
  • The presence of stigma might therefore act as a deterrent towards “non-normal” behavior!
  • The construction of large prison like Victorian mental institutions support this theory
  • Their continued use might reinforce our perception that mentally ill people are dangerous and require treatment in a secure environment
93
Q

what are we doing about ental health stigma

A

• Normalising treatment

  • The move from asylums to wards in general hospitals.
  • The move from hospital to community care
  • The tiering of services and normalisation of mild/moderate conditions such as depression and anxiety

• Reviewing Legislation

  • The growing evidence base and ongoing research, informs us that we need to treat people as individuals, collaboratively within evidence based pathways of care if we’re to get the best outcomes
  • The new western Australia mental health act and similar reviews of legislation in Australia reflect this growing evidence by placing greater emphasis on patient collaboration and advocacy, challenging the traditional medical model of psychiatry

A shift in public perception
• The growth of user groups and NFP charitable organizations, moving mental illness and wellbeing into public domain and accessible to all. Beyond Blue, mindfulness groups in libraries and schools, education, awareness and understanding

And finally,…
Research suggests that media and reporting are becoming more responsible when depicting mental illness
Attitudes are changing with a swing towards “counter stigma”

94
Q

why is it important to recoginse mental health stigma in nursing

A
  • Regardless of your area of work, its important to understand what evidence tells us about stigma
  • Stigma has a negative impact on outcome… So why would any nurse do something to a patient that makes their condition worse
  • Empathy, compassion and understanding challenge stigma
95
Q

2 broad categories of severe and enduring mental illnesses

A

1- Psychotic illness:
Different types of schizophrenia
Bi-polar affective disorder
Other types of psychotic illness, for example drug induced psychosis, psychotic depression.
2. Acute disorders that move between moderate and severe
For example: Very severe depression with suicidal intent
Severe cases of anxiety where the condition has become chronic and debilitating
Other common disorders where there is significant risk.

96
Q

myths of scitzophrenia

A

Schizophrenia means splitting of the mind, which makes the person flit from one personality to another.. Like Jekyl and Hyde”..
 Schizophrenia is not a splitting of the mind. It is characterised by the presence of psychosis a state in which a persons reasoning and thinking are distorted, leading to a loss of contact with reality.
 “People with schizophrenia are possessed by the devil!..”
 An old belief, but one that still influences our thinking.. probably deriving from the common feature of people with schizophrenia hearing voices (auditory hallucinations), which are sometimes quite commanding.
 People with schizophrenia are all locked up in mental wards where they’re regularly secluded in padded cells and given lots of electric shock treatment”..
 The introduction of new, very specific medications means that the average hospital stay for someone with schizophrenia is 23 days. Because of this change, most acute mental health wards are open wards, not locked, and it is very unusual for physical restraint or seclusion to take place. The correct term for electric shock treatment is Electric Convulsive Therapy (ECT). It is not indicated for use in schizophrenia (indicated for depression).

97
Q

pathophysiology of schizophrenia

A

 Studies suggest that there is a strong genetic influence in schizophrenia
 Twin studies have shown a higher rate of schizophrenia than in the general population inferring genetic aetiology, however this is not conclusive.
 Multiple, interacting genes may be likely in the development of schizophrenia
 Recent studies suggest that a combination of genes is more likely to cause susceptibility to schizophrenia.
 Some studies have shown “genetic vulnerability”, which when coupled with a dysfunctional family can cause susceptibility to schizophrenia, suggesting the possibility of environmental and genetic interaction

 Neurodevelopmental aetiology has also been proposed
 Possible links to in-utero infection
 Structural neuroanatomical changes have been studied in people with schizophrenia, but it is unclear if these changes are causative, or resulting from the illness.

 The “dopamine hypothesis” suggests that the psychotic symptoms of schizophrenia are a result of excess dopamine activity in the synapse.
 During an acute episode of psychosis, the effects of dopamine outweigh the effects of acetylcholine
 Increased dopamine result in “positive symptoms”

98
Q

symptoms of scitzophrenia

A

 We refer to the symptoms of schizophrenia as falling into two distinct categories;
Positive Symptoms, which are an exaggeration or distortion of normal function
Negative Symptoms, characterized by the reduction in normal functioning.

99
Q

positive symptoms of scizophrenia

A

 Hallucinations; commonly auditory. Most people with schizophrenia hear voices or noises in their head. Many also have visual, olfactory and tactile hallucinations.
 Thought disorders such as delusion (illogical or incoherent thinking)
 Disorganised speech and behaviour.

100
Q

negative symptoms of scizophrenia

A
	Apathy
	Lack of motivation
	Reduction in energy
	Low mood and depression
	Social inactivity
	Isolation
	Loss of pleasure
101
Q

phases of scizophrenia

A

1) Prodromal
2) Acute
3) Chronic

102
Q

describe phases of scizophrenia

A
Prodromal phase
	Commonly starts in adolescence.
	Characterised by loss of function
     - Social functioning
     - Organisation
     - Intellectual
     - Performing physical activity
Many parents interpret these as normal stages of adolescence, and schizophrenia is rarely diagnosed at this stage without the emergence of acute symptoms.
Acute phase
	Characterized by distortion of perception and further loss of functioning.
 - Hallucinations
 - Delusions
 - Decreased self-care
 - Isolation
 - Acute distress and anxiety

Chronic phase
 Characterized by the “burnout” of positive symptoms and increase in negative symptoms:
- Social Isolation
- “Poverty of ideas”
- “Poverty of speech”
The chronic phase might also be a feature of the long term use of older style anti-psychotic medication and major tranquilizers reducing dopamine activity in the frontal cortex of the brain.

103
Q

treatment of schizophrenia

A
  • Pharmacological therapy
  • Occupational Therapy
  • Physiotherapy
  • Cognitive Behavioural Therapy
  • Social and Welfare needs
  • Educational and career support
  • Ongoing support with physical health
104
Q

what is pain

A

Pain is unpleasant regardless of the trigger the experience is likely to be negative. Pain is a sensory experience; we can define the site and stimulus and distinguish between different types and intensities of pain
 The negative physical sensation of pain will also trigger an emotional response; for example, anxiety, fear or sadness.
 The emotional (affective) response will produce a behavioral or motivational change; for example.. moving ourselves away from the source.
 The emotional/behavioral aspects of pain are referred to as the affective-motivational aspect of pain.

another definition…
 Pain is caused by “actual or potential” tissue damage.
 Actual being a cut, bruise, burn etc., to tissue.
 Potential: arising from a stimulus without tissue damage; for example, touching something hot without actually causing tissue damage
 Pain can also be experienced when there is no stimulus or actual damage to tissue.
 Such pain is caused by damage to the central or peripheral nervous system.
 There are other known factors causing variations to the experience of pain: cognitive, social and environmental. Natural analgesia (endorphins) when triggered by these factors will modify the experience of pain.
For example, it’s likely to trigger the endorphins and reduce the level of pain we experience if we get rid of negative thoughts and think of a good one, be on a beach or somewhere nice and/ or be able to meditate.

105
Q

affective motivational aspects of pain

A

physical sensaion
emotional response
behavioural response

106
Q

types of pain

A

 Nociceptive pain
This is pain arising from actual or threatened damage to non-neural structures; bumps, cuts and burns to tissue.

 Neuropathic pain
Caused by injury or disease of the central or peripheral nervous system

107
Q

what is acute and chronic pain

A

 Acute Pain
Pain that lasts up to three months.. most commonly nociceptive pain
 Chronic Pain
Pain that lasts for more than 3 months; usually neuropathic
when acute moves on to chronic pain usually an indication that the analgesia is not working effectively for the patient and needs to start looking for an alternative pain relief.

108
Q

what is referred pain

A

 Referred pain

Pain that is experienced in a different location to the source

109
Q

what is hyperalgesia

A

 An increased response to a stimulus that’s normally painful.

110
Q

what is allodynia

A

 Pain due to a stimulus not normally causing pain.
 Breakthrough Pain
 Usually referred to in terms of cancer patients where pain breaks through the opiate analgesia, and breakthrough analgesia or a continuous release opiate is required.

111
Q

what is incident pain

A

 Incident Pain

 Where procedures, dressings etc., stimulate the damaged area and increase the pain experience

112
Q

overview of physiology of pain

A

The physiology and pathophysiology of pain will be explored in greater detail in following lectures, however the sensation of pain is carried along three neuronal pain pathways.
 The first order neurons carry information from the injured tissue to the peripheral nervous system.
 The second order neurons carry information up the spinal cord to the CNS.
 The third order neurons then distribute the information to the cerebral cortex and the individual becomes aware of the pain.

113
Q

limbic systems role in pain resposne

A

The limbic system is the portion of the brain that deals with three key functions: emotions, memories and arousal (or stimulation).

114
Q

what are neuromodulators of pain

A

Neuromodulators of pain
Several substances are capable of altering the pain pathways; these are referred to as “neuromodulators”

Neuromodulators will excite or inhibit nerve transmission.
 Glutamate (ex)
 Endorphins (in)
Neuromodulators are modulators of pain. It occurs naturally in the brain e.g. endorphins which will inhibit nerve transmission. Endorphins are usually released to help with anxiety and modulate and inhibit nerve transmission.
Glutamate which will make it excite, you feel pain more significantly when glutamate is released.

115
Q

describe presentation of pain

A

 Pain is complex and highly subjective. No two people will have the same experience of a stimulus. Individual variables include
 Differences in pain tolerance.
 The pain threshold.
 Autonomic and sympathetic nervous system activation.

116
Q

describe pain accross the lifespan

A

 Evidence suggests that infants feel
pain, however pain management in
infants remain a challenge because
of their inability to communicate.
 Assessment tools including the Face Legs Activity Cry Consolability (FLACC) scale have been developed
 It is thought that our sensitivity to pain increases as we reach adolescence

Develop ways in assessing people’s pain and especially when they are unable to communicate
Various of assessment has been developed to help us.
- FLACC (develop specifically for children)

Good way of assessing an infant AND measuring pain from a baseline and assessing whether e.g. analgesia has been effective.

117
Q

elderly and pain

A

 The elderly typically experiences greater levels of pain.
 Changes in thickness of
skin as we age.
 Development of peripheral
neuropathies.
 Co-morbidity with cognitive decline and chronic disease.
 Reluctance to take medications.

118
Q

considerations during assessment of pain

A

 Given that there are so many variables that might influence individual perception of pain; the evaluation of pain is often difficult.
 “Listen to and believe” what a patient says about their pain.
Pain is totally individual, and experience is very individual as well. Therefore, it is important to believe what the patient is saying even if it looks like a very minor injury.
 Location, type and duration descriptions.

 Pain measurement tools

119
Q

pain meaurement tool examples

A

Pain intensity scale

  • Facial pain scales
120
Q

pharmacological treatments of pain

A

 Analgesics
 Mild pain – paracetamol
 and Nonsteroidal
 anti-inflammatory drugs
 (NSAIDs)
 Moderate pain – weak opioids (e.g. tramadol)
 Severe pain – strong opioids (e.g. morphine, oxycodone)

121
Q

biomedical treatments of pain

A

 Surgery including midline myelotomy (Midline myelotomy is part of the nerve that carries signal, the transmission)
 Injections e.g. steroid injections and local anaesthetic blocks.
 Stimulation techniques such as ActivBody TENS machine (TENS), acupuncture and spinal cord stimulation.
 Physical and manual therapies such as manipulation and massage.

122
Q

psychological approaches to pain

A

 Psychological education
Any education you provide the patient about their pain will help them to manage it themselves and help them to reduce the pain experience.
 Relaxation, meditation and visualisation techniques.
This will help aid and reduce pain experience.
 Cognitive Behavioural Therapy
Thinking of nice thoughts can reduce the experience of pain.
Things like our beliefs about pain, our assumption about our pain is going to have an impact on your emotional experience which will then trigger behaviour and often physiological responses and more pain. Therefore, if we know we can control change or distinguish between helpful and unhelpful cognition we can adapt and monitor our behavioural response.

123
Q

describe nocireceptors

A

 Nociceptors are nerve receptors that are sensitive to pain.
 They give an immediate response when stimulated.
 Situated at the ends of small neurons woven throughout the tissue of the body.
 Pain occurs when nociceptors are stimulated.
 Intensity and duration of stimuli will determine the sensation.

124
Q

describe neuron types

A

 We have two types of neuron in the peripheral nervous system.
 Sensory: Neurons through which pain is perceived
 Motor: Neurons which respond to pain < Help us to move our body.
 Sensory neurons connect (synapse) with the spinal cord which then synapse within the CNS.

125
Q

dsecribe ascending order pathways first order

A

Pain is perceived by nociceptors which transmit signals through…
 A-delta fibres: which respond quickly to sharp pain.
 C fibre: which are smaller in diameter, slower, and respond to dull, aching pain.
They transmit in the dorsal horn to the
Second order

126
Q

describe second order neuron pathway

A

 The A-delta and C fibres transmit impulses to second order sensory neurons through the dorsal horn of the spinal cord where they synapse.
 Fast pain (A-delta) then ascend via the anterior spinothalamic tract.
 Slow pain (C fibres), ascend via the lateral spinothalamic tract.
 The spinothalamic tracts terminate in the thalamus.

127
Q

describe third order neuron pathway

A

 Third order neurons in the thalamus then transmit the impulse to the cerebral cortex.
 Here it is perceived, interpreted and pain is experienced, alerting the person to injury requiring a response.

Synapse >between the 2nd and the 3rd order in the thalamus

128
Q

what is the The Paleospinalthalamic tract.

A

The Paleospinalthalamic tract.
 Some pain impulses make their way up the paleospinothalamic tract to the limbic system.
 The limbic system is the area of the brain which formulates cognitive and emotional responses and is known to play a large role in the processing of trauma.
 This integrates the emotional, cognitive and autonomic responses to pain.

129
Q

 When damage occurs to the peripheral or central nervous system, this will result in what type of pain

A

neuropathic pain.
 Neuropathic pain can be acute; for example, in the case of a trapped nerve or chronic due to disease or changes in the nervous system.
 Causes of neuropathic pain are numerous
- Trauma
- Surgery
- Inflammation
- Neuropathies (Diabetic, HIV, tumour related)

130
Q

pain theories

A

gate control theory
neuromatrix
central sensitization
central sensitization/ dysfunctional pain

131
Q

define homeostaisis

A

Homeostasis: the body maintaining a stable constant condition despite changes in the environment
Numerous mechanisms are involved, that can act simultaneously or successively

132
Q

why have reference ranges

A
  • Our bodies need to be able to recognise what is a normal or abnormal variable to maintain homeostasis
  • These are the ‘normal’ ranges (no 2 people are the same but should be within these ranges)
133
Q

describe homeostais at a cellular level

A

constant movement of nutrients, fluids and ions between cellular membrane and blood
- a cell maintains its own consistent internal environment, pumping/ draeing nutrients in or out as required

134
Q

decribe maintanance of Level of ions

A
  • Levels of ions need to be maintained to ensure normal cell function
  • Sodium, potassium and calcium are particularly important for neurons to function as nerve cells
  • Fluctuation can also cause cardiac excitability and abnormal heart rhythm during conduction in cardiac system

Sodium (Na+)- IC: Low EC: High
Potassium (K+)- IC: High EC: Low
Calcium (Ca²+)- IC- Low EC: High

135
Q

RELEX loop of pain response

A
hand  touches sharp
detected by neurons in hand
processed by control center in spinal cordeffector or output by effector muscles to arm muscles causing
move hand away quickly leading to
prevention of futher damage
136
Q

homeostasis at body level

A
  • Requires the coordination of multiple body systems including the renal system, central nervous system and endocrine system
  • Can see system when these loops become overwhealmed
137
Q

components of negative feedbaclk loop

A
  • Sensor: neuron that is able to detect changes in the variable concerned eg. Pain, bsl
  • Control centre: CNS that matches information sent from the sensor with the reference range to decide if a response is required
  • Effector: send a message to the appropriate region of the body to mediate the response required
138
Q

carbon dioxide build up feed back loop

A

build up of carbon doxide
sensed by neurons in brain and major blood vessels
neural signals to the brain sent
control center in brain compare actual carbon dioxide levels with normal ranges; corrections are requires
neuron signals from the brain to effector signals to lungs to cause increased breathing which leads to more carbon dioxide being exhaled

139
Q

what is shock

A

a clinical condition in which there is an imbalance between oxygen supply and demand which results inadequate blood flow to organs and tissues causing life threatening cellular dysfunction

140
Q

effect of shock on cellular processes

A
  1. ATP can only be produced by anaerobic glycolysis which results in lactic acidosis
  2. The heat produced as a by product of the use of ATP is dramatically reduced
  3. Tissue damage and associated inflammatory response.
141
Q

types of shock

A
hypo volemic
cardiogenic
neurogenic
septic
anaphylactic
142
Q

mechanis,m of hypovolemic shock

A

decreased intravascular volume = decreased preload= decreased cardiac output= moves shift of interstitial fluid, ADH stimulation, splenic discharge= increased volume= cardiac output= volume loss causing decreased cardiac output= decreased perfusion and cellular metabolism

143
Q

clinical manifestions and management of of hypovolemic shock

A
  • Poor skin turgor
  • Thirst
  • Oliguria
  • Tachycardia
  • Thready pulse
  • Deterioration in mental status – confusion, drowsy
  • Can determine if vasoconstriction is occurring to compensate if there is a rise in diastolic pressure or if peripheral pulse decreased in strength

Management
• Rapid fluid replacement

144
Q

what is cardiogenic shock

A
  • caused by decreased cardiac output and tissue hypoxia however there is adequate blood volume
  • may happen when there is muscle damaged following an acute MI
145
Q

mechanim of action for cardiogenic shock

A

decreased cardiac output= stimulates release of Compensatory renin aldosterone, ADH == shifts adequate or increased blood volme= Increase preload, SV, HR

Decreased cardiac output also stimulates release of adrenaline and noradrenaline compensatory release= increased SVR and increased preloas, SV and HR

Increased Preload, SV,HR= myocardial o2 req= decreased cardiac output, decreased ejection fraction (lowering BP)= decreasing tissue perfuson= impaired cellular metabolism

146
Q

clinical manifestations and management of cardiogenic shock

A

Clinical manifestations
• Blood Pressure: hypotension
• Pulse: rapid, thready, distension of neck and hand veins
• Respirations: increased, laboured, crackles and wheezes, pulmonary oedema
• Skin: pale, cyanotic, cold, moist
• Mental Status: restless, anxious, lethargic progressing to comatose
• Urine Output: oliguria to anuria
• Other: dependent oedema, elevated CVP, arrhythmias

Management
•	Fluid administration (carefully to support BP as blood volume may not be low)
•	Catecholamine administration
o	Adrenaline
o	Noradrenaline
o	Dobutamine
147
Q

Neurogenic shock

A

Results in widespread vasodilation from overstimulation of parasympathetic nervous system or under stimulation of the sympathetic nervous system. Can be caused by trauma in spinal cord or any conditions that interrupt oxygenation to the medulla.

Vessels vasodilate= hypotension and relative hypovolemia
Relative hypovolemia: because vessels have dilated, we still have same BV but needs to fill larger diameter of vessel = less pressure circulating = bp drops

148
Q

mechanism of action neurogenic shock

A

decreased sympathestic and or increased parasympathetic response= decreased vascular tone= massive vasodilation= decreased systemic vascular resistence= inadequate cardiac output= decreased tissue perfusion= impaired cellular metabolism

149
Q

manifestations and management of neurogenic shock

A
Manifestations
•	Blood Pressure: hypotension
•	Pulse: slow and bounding
•	Respirations: vary
•	Skin: warm and dry
•	Mental Status: anxious, restless, lethargic progressing to comatose
•	Urine Output: oliguria to anuria
•	Other: lowered body temperature

Management
• Careful use of fluids to increase bp
• Vasopressors to constrict the vessels

150
Q

what is septic shock

A
  • One component of systemic inflammatory response
  • Begins with an infection which causes bacteria to enter the bloodstream progressing from sepsis to septic shock
  • High mortality rate 23% in hospital
  • Most common causes are pneumonia and urinary tract infection
151
Q

mechanism of septic shock

A

bacteramia= as gram negative or gram positive organism.
gram negative= release endotoxins, gram positive= release exotoxins

endotoxins and exotoxins act as triggering molecules activating= complement systems, coagulation cascade, kinin sysntem, neutrophil, endothelial and monocyte macrophage cell acivity= release of central endogenous mediators= tumor necrosis factor alpha= release of proinflammatry cytocines= endothelial damage= a number of responses eg. hypotension, decreased systemic vascular resistence, decreased myocardial function= organ dysfunction