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NUR 305 exam prep Sam Fox Flashcards

1
Q

Name the four components of psychological patient care

A
  1. Anxiety
  2. Delirium
  3. Pain
  4. Sleep
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2
Q

Name six precipitating factors of anxiety

A
  1. Concern about current illness/underlying chronic disease
  2. Current experiences and feelings
  3. Current care interventions
  4. Medication side effects
  5. Environmental considerations
  6. Concern about ongoing impact of illness on recovery
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3
Q

List four reasons why patients may have anxiety

A
  1. Patient is overly dependent on the nurse
  2. Are occupied with internal dialog
  3. Have a long term recovery ahead
  4. Perceive treat to their wellbeing
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4
Q

List four contributing factors of anxiety

A
  1. Duration and severity of illness
  2. Loss of sense of control
  3. Impact of illness on the family
  4. Frequency and complexity of invasion interventions
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5
Q

List and briefly discuss two types of anxiety management

A
  1. Pharmacological treatment – treat pain & any other reversible psychological causes of anxiety and agitation
  2. Non-Pharmacological treatment – such as: massage, music therapy & noise reduction
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6
Q

Sleep deprivation in patients who are critically ill is often attributed to:

a) Bed baths during the evening shift
b) Untreated pain & anxiety
c) Family visiting
d) Altered melatonin levels

A

b) Untreated pain & anxiety

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7
Q

Discuss how nurses can help promote patients sleep

A

Plan treatments together, daily baths to suit the patients requirements, reduce environmental noise, encourage quiet time, reduce lighting and interventions.

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8
Q

What are the normal ABG values?

A

pH 7.36 - 7.44

PaC02 35 - 45 mmHg

Pa02 80 - 100 mmHg

HC03 22 - 32 mmEq/L

Base excess + - 3 Eq/L

Sa02 > 94%

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9
Q

Interpret the following:

pH - 7.48

PaC02 - 30 mmHg

Pa02 - 90 mmHg

HC03 - 24 mmEq/L

Sa02 - 98%

A

pH = >

PaC02 =

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10
Q

Acidosis / alkalosis readings =

A

acidosis alkalosis
6.8 8
= =
Death Death

pH homeostasis = 7.36 - 7.44

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11
Q

Metabolic readings:

A

pH and C02 go in equal direction = metabolic

pH, > C02 =
metabolic alkalosis

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12
Q

Respiratory readings:

A

pH and C02 go in opposite directions = respiratory

C02 =
Respiratory acidosis

> pH,

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13
Q

R.O.M.E stands for?

A

Respiratory
Opposite
Metabolic
Equal

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14
Q

Recognition of uncompensated blood values:

A

If pH, PaC02 and HC03 are abnormal

uncompensated

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15
Q

Recognition of compensated blood values:

A

If pH is normal - but - PaC02 and HC03 are abnormal
=
Compensated

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16
Q

Ventilation (VQ) Perfusion ratio

A
  • Ventilation and perfusion differ depending on the region of the lung. On average, the alveolar ventilation is about 4 L/min.
  • Normal pulmonary capillary blood flow is about 5 L/min
  • Therefore, ventilation/perfusion ratio is 4:5, or 0.8. (VQ = 0.8)
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17
Q

Metabolic Acidosis S and S:

A

β€’ resp rate and depth,

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18
Q

Metabolic Alkalosis, S and S:

A
  • > pH > Bicarbonate
  • > bicarbonate in the ECF
  • Commonly due to vomiting, gastric suction, long term diuretics = fluid loss
  • Hypokalaemia produces alkalosis
  • S and S:
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19
Q

Respiratory Acidosis, S and S:

A
  • PaCO2
  • > Carbonic acid in the ECF
  • Due to resp problem with inadequate excretion of CO2 (COPD)
  • Body may compensate or may to asymptomatic
  • S and S: > HR, > RR, > BP, mental changes, feeling of fullness in head, >? intracranial pressure, alveolar hypoventilation, alveolar hyperventilation, mechanical ventilation, inadequate perfusion
  • Treatment: need to improve ventilation
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20
Q

Respiratory Alkalosis, S and S:

A

β€’ > pH,

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21
Q

What are the two different types of oxygen delivery systems?

A
  1. High flow oxygen system – venturi mask
    β€’ Guarantees FI02 irrespective of breathing pattern
    β€’ High & low concentrations are possible
  2. Low flow oxygen system – all other devices
    β€’ Mixes with room air
    β€’ Is influenced by breathing pattern
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22
Q

Disassociation curve:

A
  • In the tissues the oxygen – haemoglobin dissociation curve shifts to the right as the pH increases or temperature rises
  • In the lungs, the oxygen – haemoglobin dissociation curve shifts to the left as the pH increases or the temperature falls resulting in an increased ability of haemoglobin to pick up oxygen
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23
Q

Disassociation curve:

A

In the TISSUE the oxygen – haemoglobin dissociation curve shifts to the RIGHT as the pH increases or temperature rises
= lower affinity for oxygen (not good)
β€’ In the LUNGS, the oxygen – haemoglobin dissociation curve shifts to the LEFT as the pH increases or the temperature falls resulting in an increased ability of haemoglobin to pick up oxygen
= the greater the affiniuty for oxygen (good)

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24
Q

CPAP (Continuous Positive Airway Pressure)

A
  • Support for spontaneously breathing patients & ventilated patients
  • Non-invasive via a mask
  • Addition to mechanical ventilation
  • Raised positive pressure assists in reducing the work of breathing on inspiration
  • Increases gas exchange and reduces hypoxia
  • Commonly used in patients with: pulmonary oedema, COPD & asthma

While CPAP generally delivers a single pressure, BiPAP delivers an inhale pressure and an exhale pressure

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25
Q

BiPAP (Bilevel positive airway pressure)

A

Involves:
IPAP (Inspiratory positive airway pressure
β€’ A higher pressure is delivered on inspiration
EPAP (Expiratory positive airway pressure)
β€’ Lower pressure but still positive on expiration

BiPAP is sometimes used in patients who have pulmonary lung issues, like COPD. The difference in pressures helps to eliminate extra CO2 carbon dioxide gas from the body.

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26
Q

NIV, CPAP and BiPAP are all commonly used in?

A
  • High dependency patients
  • Neurological disorders ( Guillain Barre syndrome)
  • Obstructive sleep apnoea
  • COPD
  • Asthma
  • Post intubation weening issues
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27
Q

Clinical conditions for mechanical ventilation include?

A
  • Respiratory failure (type 1, post anaesthetic)
  • Acute lung injury
  • Asthma
  • Pulmonary embolism
  • Pneumonia
  • Severe acute respiratory syndrome
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28
Q

Mechanical Ventilation Parameters

A
  • Fraction of inspired 02 (Fi02) os 0.6 = 60%
  • Inspiratory : expiratory ratio
  • Tidal volume / minute volume
  • Ventilator breath rate
  • Pressure support
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29
Q

Type 1 and type 2 respiratory failure

A 
Type 1:
Post anesthetic
Lung injury
Asthma 
Pneumothorax (collection of air in the cavity causing the lung to collapse) 
Pneumonia 
Type 2:
Asthma
COPD
Upper airway
Obstruction
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30
Q

Clinical markers of shock:

A
  • Lactate & acid base disturbances
  • Need to assess – ABG, pH, base excess
  • Increased lactate is a warning sign of organ failure
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31
Q

02 delivery

A

Nasal canula 2 - 4L/min
25 - 45%

Venturi 4 - 8 L/min
24 - 50% (COPD)

Hudson 6 - 10/Lmin
40 - 60%

Non-rebreather 10 - 15 L/min
60 - 100%

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32
Q

Clinical markers of shock:

A
  • Lactate & acid base disturbances
  • Need to assess – ABG, pH, base excess
  • Increased lactate is a warning sign of organ failure
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33
Q

definition of shock?

A

Homeostatic imbalance occurs between nutrient supply and demand

Is the inability of the body to meet the metabolic demands of the tissues = hypoperfusion (the amount of 02 reaching the cells)

Adaptive responses can no longer accommodate circulatory changes

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34
Q

Clinical markers of shock:

A
  • Lactate & acid base disturbances
  • Need to assess – ABG, pH, base excess
  • Increased lactate is a warning sign of organ failure
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35
Q

List the early indicators of shock

A
  1. Tachycardia
  2. Altered GCS
  3. Cold skin
  4. Tachypnoea
  5. Shallow resps
    6.
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36
Q

There are five main sites for significant blood loss:

β€œon the floor and 4 more”

A

a.) external haemorrhage.
b.) in the chest i.e. haemothorax.
c.) in the abdomen. Spleen and liver are common.
d.) pelvic fractures.
e.) long bone fractures.
Feel: Skin temp., capillary refill. Pulse rate and volume.
(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.

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37
Q

There are five main sites for significant blood loss:

β€œon the floor and 4 more”

A

a. ) external haemorrhage.
b. ) in the chest i.e. haemothorax.
c. ) in the abdomen. Spleen and liver are common.
d. ) pelvic fractures.
e. ) long bone fractures.

Feel: Skin temp., capillary refill. Pulse rate and volume.

(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.

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38
Q

There are five main sites for significant blood loss:

β€œon the floor and 4 more”

A

a.) external haemorrhage

If blood is not on the floor it could be….

b. ) in the chest i.e. haemothorax
c. ) in the abdomen. Spleen and liver are common
d. ) pelvic fractures
e. ) long bone fractures

Feel: Skin temp., capillary refill. Pulse rate and volume.

(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.

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39
Q

Name the types of shock

A
  1. Hypovolemic
  2. Cardiogenic
  3. Distributive shock:
    β€’ Sepsis
    β€’ Anaphylaxis
    β€’ Neurogenic
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40
Q

Identifying types of shock:

A

Primary Survey: A – E assessment

Secondary Survey – top to toe

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41
Q

Identifying types of shock:

A

Primary Survey: A – E assessment

Secondary Survey – top to toe

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42
Q

Hypovolemic Shock:

A
  • Low volume of blood or fluid – bleeding (internal/external), vomiting, diarrhoea, burns, dehydration
  • Most common cause is bleeding
  • Easy to diagnose & treat
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43
Q

Treatment of hypovolemic shock:

A
  • Rapid A - E
  • Secure airway/breathing
  • Fluid resuscitation
  • Increase preload - cardiac output
  • minimize further fluid loss
  • Fluid infused to reflect loss (burns = plasma, hemorrhage = blood/colloid/crystalloid) to maintain agreed MAP and SBP
  • NOTE: can cause overload- need to monitor ABGs, Vitals, cap refill
  • Keep patient warm
  • Bolus dose = Vol/Kg
  • Prepare for theatre
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44
Q

Cardiogenic Shock

A

β€’ Is the inability to maintain adequate perfusion despite adequate circulatory volume

02 is not clinging to the molecules and therefore, not reaching the tissue

Shift to right of dis curve = high affinity

Base excess is out of normal range (+- 3) = compensating
(body has used up all compensatory mechanisms) = deterioration

  • Increase lactate = warning sign of organ failure

β€’ Difficult to diagnose
β€’ Usually occurs within 48 hrs after a MI
β€’ Main cause if left ventricular failure
- Mortality 50 - 80%

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45
Q

Cardiogenic shock S and S:

A
  • Low cardiac output
  • Sever pulmonary congestion (feel like drowning)
  • Hypotension 10 sec
  • Anxiety
  • Dyspnea (
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46
Q

Cardiogenic treatment:

A
  • Multi system approach
  • Frequent assessments
  • Increase oxygen supply – CPAP / BiPAP as required
  • Decrease physical activity
  • Holistic care & support
  • ?fluids
  • Inotropes
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47
Q

Inotropes:

A

Inotropes are a group of drugs that alter the contractility of the heart. Positive inotropes increase the force of contraction of the heart, whereas negative inotropes weaken it.
Inotropes are indicated in acute conditions where there is low cardiac output (CO), such as cardiogenic shock following myocardial infarction, acute decompensated heart failure and low CO states after cardiac surgery.
Reduced CO leads to tissue hypo-perfusion and subsequent hypoxia. Metabolism switches from aerobic to anaerobic, resulting in the formation of lactic acid. If left untreated, this can result in multi-organ failure and death

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48
Q

Disruptive shock

A 
β€’	Tissue has impaired oxygen & nutrient delivery  
β€’	Failure of the vascular system 
β€’	Leading to widespread vasodilation 
	Septic shock
	Anaphylaxis
	Neurogenic
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49
Q

Septic Shock

A

β€’ Is systematic inflammation –
Caused by – sepsis, burns, pancreatitis, trauma
β€’ restricts blood flow
β€’ oxygen delivery to tissue is compromised
β€’ cardiac output increases
β€’ hypovolemia occurs – the blood dilates & distributes
β€’ the patient will need >fluid to accommodate tissue = which is bad, the blood will continue to expand & the patient will become over loaded
β€’ patient will present – warm, pink & well perfused
β€’ decompensation will lead to cell death & multiple organ failure

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50
Q

Treatment for septic shock

A

similar to hypovolemia, assess, fluid management, treat underlying infection, administer inotrope vasopressin

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51
Q

Anaphylaxis

A

β€’ severe allergic reaction
β€’ 1st expose to the allergen – no anaphylaxis (poss reaction)
β€’ 2nd exposure to allergen = anaphylaxis
Patient may present - anxiety, dizzy, faint, stridor (high pitch sound), wheeze, tachypnoea, dyspnoea (SOB), pharyl/laryngeal oedema, bronchospasm, cyanosis, tachycardia, hypotension, arrhythmias, N & V, diarrhoea, rash, itchy, erythema

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52
Q

Anaphylaxis treatment

A

Rapid A - E

  • Adrenaline
  • Antihistamine
  • Corticosteriods
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53
Q

Neurogenic shock

A
  • spinal shock
    β€’ Spinal cord injury above T6
    β€’ Commonly caused by trauma
    β€’ Loss of vasomotor tone – disruption to neural output
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54
Q

Neurogenic shock S and S:

A

Hypotension ( HR does NOT occur

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55
Q

Neurogenic treatment

A
  • ABC
  • Stabilise neck & torso
  • Fluids if needed
  • Resp assessment (risk of pneumonia & atelectasis
  • Maintain core temp
  • Initiate NBM
  • Pressure area care
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56
Q

Name four areas of nursing care for shocked patients

A
  1. Rapid A – E
  2. Holistic care – involve family
  3. Communication – patient, staff, family
  4. Interventions – fluids, obs, scribe, meds, transfer
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57
Q

Remember VIP - shock

A

Ventilation - airway, added and ventilation

Infusion - of appropriate volume expanders

Pumping - improve heart pumping with drugs - antiarrythmics, inotropes, diurectics, vasodilators

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58
Q

Patient assessments for shock

A
  1. Cardiovascular
  2. Neurological
  3. Renal function - insert catheter to measure urine output
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59
Q

Observations for shock include:

A 
Resps,
Temp,
HR, 
BP, 
Sa02,
U/o, 
GCS,
ABGs, 
- bloods to measure lactate = > lactate warning sign of organ failure 
cardiac output – central line
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60
Q

Vasopressors:

A

class of drugs that evlevate mean arterial pressure by inducing vasoconstriction

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61
Q

common inotropes

A

Heart failure:

  • Dobutamine
  • Dopamine

Septic shock, Cariogenic shock, anaphlatic shock, neurogenic shock and hypotension (following anesthethic):

  • Adrenaline - Epinephrine
  • Phenlepfine
  • Noradrenaline

second line agent for septic and anaphlatic:
- Vasopressin

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62
Q

Treatment pathway for shock

A 
fluid resus
medication management
theartre
rehab
transfer - ICU, spinal unit
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63
Q

Cardiac conduction system

A
  1. Sinoatrial - SA node (pacemaker) fires
  2. excitation spreads through atrial myocardium
  3. Atrioventricular - AV node fires
  4. Excitation spreads down AV bundle
  5. Perkinje fibres distribute excitation through ventricular myocardium
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64
Q

Need to find where the blockage is to know the extent of damage

A
  • large arteries = > damage

* artery branches =

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65
Q

Cardiac output

A
  • the amount of blood pumped by the heart each minute
  • regulated by homeostatic mechanisms
  • regulated in response to stress & disease
  • is affected by preload, afterload & contractility
  • critically ill patients do not compensate as well as healthy people
  • maybe unable to >HR to compensate BP & hypertension
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66
Q

Cardiac output - CO =

A

HR x Stroke volume

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67
Q

Stroke Volume

A

β€’ the volume of blood pumped with heart beat (50-100ml/beat)

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68
Q

Preload

A

Pressure of stretch exerted on the walls of the ventricle by the volume of blood filling the ventricles at the end of diastole; used as an indication of volume status

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69
Q

Factors that can reduce preload:

A
  • volume loss – haemorrhage
  • venous dilation – hyperthermia / medication
  • tachycardia’s AF / super ventricular tachycardia (SVT)
  • raised intrathoracic pressure – need to use NIV, BiPAP, CPAP
  • raised intracardiac pressure – tamponade - Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium).
  • Body position can affect preload due to the effect on venous return
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70
Q

Central venous pressure (CVP)

A

β€’ Preload of the right ventricle measured by the CVP

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71
Q

Contractility

A

The ability of a muscle to shorten when stimulated; in particular the force of the myocardial contraction
β€’ Is difficult to measure clinically
β€’ Decreased by:
1. Hypoxia Both cause MI’s
2. Ischemia
3. Drugs: thiopentone, calcium channel blockers
β€’ Increasing contractility will increase myocardial oxygen demand

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72
Q

Mean Arterial Pressure (MAP)

A

β€’ Average pressure within the arterial system throughout the cardiac cycle 70 – 90 mmHg

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73
Q

Assessment of CO & haemodynamic monitoring

A
  • Establish Dx
  • Determine therapy & monitor response to it
  • Heart rate & rhythm - 4 or 5 lead or 12 lead ECG
  • Non- invasive monitoring – obs, check all pulses (don’t just relay on monitors)
  • Invasive – catheter – arterial pressure monitoring, central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure
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74
Q

ECG - Calculate the rate:

A
  • Count the number of large boxes between R to the next R

* Divide 300 by the number of large squares

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75
Q

Electrical activity with the associated ECG pattern

A 
Atrial Depolarization 
= P wave 
Delay at AV node
= PR segmant
Ventricular Depolarization
= QRS complex
Ventricular Repolarisation
= T wave
No electrical activity
= Isoelectric line (the flat line at the end before it starts again)
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76
Q

Causes of chest pain - cardiovascular

A 
Myocardial ischaemia
Coronary artery spasm (angina)
Myocardial infarction
Pericarditis
Pulmonary embolism 
Mitral valve proplapse
Ca - usually secondary cancer
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77
Q

Causes of chest pain - Non-cardiovascular

A 
Dissecting thoracic aneurysm
Herpes zoster
Oesophageal reflus and spasm
Hiatus hernia
Pneumonia 
Pneumonthorax
Pleurisy
Peptic unlceration
Gallbladder disease
Musculoskeletal pain
Costochondritis
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78
Q

Costochondritis

A
  • Inflammation of the intercostal muscles
  • Musculoskeletal pain 10/10
  • Non-specific, non-localised (everywhere)
  • Resembles MI but clear ECG
  • Non-reactive to morphine
  • Need I’m ibroprofen
  • Skin is pale & sweaty
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79
Q

Stable angina

A

β€’ Often relieved by rest alone

Symptoms – chest discomfort

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80
Q

Unstable angina

A

β€’ May come on at rest

Symptoms – Acute MI (occlusion)
Sudden death

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81
Q

Management of angina

A
  • A – E assessment
  • 02 at 6L / min via Hudson mask
  • Medication as prescribed

Administer 02 b/c of the active chest pain even if sats are normal, however, studies show with holding 02 > survival rates as the body is forced to use the 02 it has in a much better way

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82
Q

Risk factors for CHD -

Non-modifiable

A 
Age
Gender
Ethnicity
Genetic predisposition
Low birth weight  
Diabetes
Hormonal/biochemical factors
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83
Q

Risk factors for CHD -

Modifiable

A 
Blood cholesterol
Tobacco smoking
High BP
Overweight/obesity
Diet
Alcohol consumption
Social class
Geographical distribution
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84
Q

Acute coronary syndrome

A

Includes all cases of unstable angina and acute MIs
Underlying pathology is the abrupt, complete or partial obstruction (occlusion) of a coronary artery
Most often triggered by the rupture of an atheromatous plaque

Nearly all deaths from CHD are the result of MI

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85
Q

Myocardial Infarction -MI

A

Arises when a region of the myocardium becomes irreversibly necrosed.
It is usually due to thromboembolic occusion of the coronary artery supplying that are of the heart muscle

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86
Q

ST elevated segment

A

All of the myocardium is being damaged

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87
Q

Chest pain assessment:

PQRST

A

P – What happened, sitting down? Running?
Q – Where is it, how does it feel, stabbing, crushing?
R – Do they have pain anywhere else? Shoulder, jaw?
S – Rating out of 10
T – When did it start?

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88
Q

MI stats

A

Each year, around 54,000 Australians suffer a heart attack.
More than 100,000 patients

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89
Q

Symptoms of MI

A 
Pain:
Chest
Left arm
Right arm
Both arms
Neck
Jaw
back

Skin:
Pale
Sweaty
Clammy
cyanosed

Respiratory:
Tachypnoea
Dyspnoeic
Pulmonary oedema

Physical signs:
Nausea
Vomiting

Psychological:
Anxiety
confusion

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90
Q

MI Dx

A

Patient History
Symptoms
ECG
Bloods

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91
Q

Obs / monitoring MI

A 
Reassure patient – rest
Baseline observations
? Need for cardiac monitoring
12 lead ECG
IV access
Troponin (T & I) levels and cardiac enzymes (CK – creatine kinase)
Contact Dr
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92
Q

MI treatment

A

Thrombolysis

PCI (Percutaneous coronary intervention) Previously called Angioplasty

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93
Q

Thromobolysis

A

The development of thrombolysis is the single most important advance in the care of coronary patients since defibrillation

Mortality is approximately 30% less than if patients are left untreated, and the NSF for CHD recommended:
Thrombolysis be given within 60 minutes of a call for help
Within 20 minutes of admission to hospital

However, Thrombolysis is now secondary treatment pathway

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94
Q

Types of thrombolytic agent

A

Streptokinase. Most widely used, and cheapest. A bacterial protein. Patients develop antibodies, and can only be given once.

Recombinant tissue-type plasminogen activator (tPA). A naturally occurring human protease that is fibrin specific and this works predominantly on the clot, with less risk of systemic bleeding

Retaplase. A new generation, appears to be as effective as streptokinase. However can be given as a bolus and is non-antigenic

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95
Q

PCI (Angioplasty) - Primary treatment pathway

A

Invasive procedure
Access through femoral artery
Catheter inserted into coronary artery
Balloon inflated in CA to open stenosed area
Stenting carried out at same time if required
Risk of cardiac arrhythmias/cardiac arrest

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96
Q

MI - A - E assessment:

A

Hx, vitals, ECG – repeated every 5 mins, ABGs, 02, IV access, chest x-ray, troponin, and reassurance

97
Q

On going care - MI

A 
Maintain safe environment 
Communication
Breathing
Eating and drinking
Elimination
Personal cleasing and dressing 
Control body temp
Mobilizing
Working ang playing
Expressing sexulaity
Sleeping 
Dying

Patient may worry if the do anything the pain will return or even die – need to help relieve anxiety

98
Q

Beneficence and non-maleficence

A

requires that nurses act in a way that promote the wellbeing of another person.

Incorporates 2 actions of doing no harm & maximising possible benefits whilst minimising possible harm (non-maleficence).

99
Q

Risk / Benefit

A

There may be times where to β€˜maximise benefits’ for positive health outcomes it is considered ethically justifiable that the patient be exposed to a β€˜higher risk of harm’ (minimised by the caregiver as much as possible).

100
Q

Informed consent

A

All treating staff are required to facilitate discussions about diagnosis, treatment options and care with the patient to enable the patient to provide informed consent

101
Q

Informed consent

A

All treating staff are required to facilitate discussions about diagnosis, treatment options and care with the patient to enable the patient to provide informed consent

Patients have the right as autonomous individuals to discuss any concerns or raise questions at any time with staff.

Because of the vulnerable nature of the critically ill individual, direct informed consent is often difficult, and surrogate consent may be the only option, particularly in an emergency.

102
Q

Advanced directives

A

For individuals who want to document their preferences regarding future healthcare decisions.

Advanced directives can only be signed by a competent person (before the onset of incompetence).

Advanced directives can therefore inform healthcare professionals how decisions are to be made, in addition to who is to make them.

Instructions given by the individual specifying what actions should be taken for their health in the event that they are no longer able to make decisions due to illness or incapacity, and appoints a person to make such decisions on their behalf.

103
Q

DNR orders

A

People with acute, reversible illness conditions should have the prerogative of resuscitation. Reflects a decision against any further proactive treatment such as β€˜CPR’.

104
Q

Identify the benefits of a systematic approach to trauma care

A

Good trauma care starts at the road side.
Results in improved survival of trauma patients.
Reduces clinical errors in the management of trauma patients.

105
Q

Discuss the different roles needed in trauma management and specifically nursing roles

A

Multidisciplinary team, Team leader who is a doctor or nurse depending on the skill set, team leader doesn’t touch the patient. Nurses will manage ABC, nurse 1 = pt’s L side nurse 2 = pt’s R side nurse 3 is a runner for fluids, packs & will be talking to the scribe nurse, specialities will be surgeon and anaesthetist.

106
Q

Discuss the primary and survey of a trauma patient

A

PRIMARY SURVEY – ABCDEF (F=Farenheit). Airway breathing & circulation take precedence. The components of the survey will occur simultaneously.

107
Q

Trauma - The priorities of care are:

A
  1. Maintaining life with priority given to airway, breathing & circulation
  2. Treating immediate problems such as bleeding
  3. Preventing complications or further compromise
108
Q

Trauma A - E

A

 Airway = risk of aspiration (blood, vomit, teeth). C Spine control in trauma cases
 Breathing = RIPPA assessment – RR, inspection, Palpation, percussion, auscultation
 Circulation = Direct pressure to control haemorrhage. Fluid resus. Haemo-dilution. – hypovolemic until proven otherwise
 Disability = AVPU (alert, voice, pain, unresponsive). Blood gases. Continuous neuro obs.
 Exposure = Remove all clothing. Log roll to check for injuries on the back of the body ( you never know what lies behind!)
 Farenheit = Hypothermia (often caused by medical staff exposing pt). Bair hugger (keeps patient warm at night), Warm fluids, Warm humidified oxygen.

109
Q

SECONDARY SURVEY of the trauma patient

A

This follows the primary survey & the patient is stabilised. This is a systematic examination of the body regions to identify injuries that have not yet been recognised.
Essential that the front and back of the patient as well as areas covered by clothing, are examined during this process. Looking for fractures, bleeding etc.

110
Q

Discuss the principles of the β€œgolden hour”

A

 In order to improve outcomes, definitive care should be provided to patients as soon as possible and preferably within 1 hour of the injury being sustained.
 In countries with large distances & sparse populations this aim presents particular challenge and cannot be met in many regions.
 Recognition of life-threatening conditions, application of appropriate emergency interventions & prompt transport to the nearest appropriate hospital remain the principles of pre-hospital care.

111
Q

PRIMARY TRANSPORT

A

from the place of injury to the first healthcare facility to provide care to the patient. This is sometimes referred to as pre hospital transport

112
Q

SECONDARY TRANSPORT

A

between healthcare facilities. Sometimes referred to as inter hospital transport and can occur via ground or air.

113
Q

SECONDARY TRANSPORT

A

between healthcare facilities. Sometimes referred to as inter hospital transport and can occur via ground or air.
 Most common cause of traumatic injury include RTA’s (road traffic accident?), falls & collisions

114
Q

Trauma Triad

A

hypothermia, acidosis, coagulopathy. (HAC)

 Can occur individually but often occur simultaneously

 Hypothermia inhibits blood coagulation which causes a build-up lactate in blood causing metabolic acidosis

 The recognition of the importance of this triad has led to the development of damage control surgery. Surgery is initiated rapidly, only the most rapid & simplest interventions that are required to stop bleeding & contamination are undertaken.

115
Q

Trauma definition

A

mechanism of injury is the energy kinetic eg: blunt or penetrating injury.
Blunt injury can be a fall or impact. Combination of forces, acceleration (how fast was the impact), deceleration (what did they hot), shearing (brain shifts from one side of the skull to the other), compression.
Penetrating injury can be a stab wound. Consider positioning & mobilisation of the patient, history (how has this happened), x rays, CT or MRI scan, hard collar (major trauma).

116
Q

BURNS CATEGORIES

A

 Thermal (electrical)
 Chemical (bleach) – cement = lime – alkaline = worst type of burn
 Radiation,
 Fire – smoke inhalation

117
Q

Discuss the incidence of burn injuries in Australia and NZ

A 
	46,000 hospitalised 1999-2004
	0-4 years scalding is most prevalent
	Males 1 in 5 are at work aged 15-39
	69% admitted between 1-3 days
	57% admitted require
118
Q

Epidermal burns

A
  • Involves the epidermis
  • Skin is pink, red and painful
  • Heals in 7 days
119
Q

Superficial Partial thickness

A

epidermis & superficial dermis – top/middle skin layer – blisters, painful, exudate – heals in 14 days

120
Q

Mid dermal partial thickness

A
  • Epidermis and dermis
  • Large zone of non -viable tissue
  • Less painful – diminished nerve endings
  • Pale to dark pink
121
Q

Deep partial thickness

A 
Waxy appearance
β€’	> risk infection
β€’	Liminted movement 
β€’	Deep into the dermis 
β€’	Pink to pale ivory colour 
β€’	Skin does not blanch
β€’	Hair falls out 
β€’	Surgically excised
122
Q

Full thickness

A
  • Epidermis and dermis destroyed, may penetrate into underlying structures
  • Dense white, waxy, charred
  • Skin often feels leathery (eschar)
123
Q

Circumferential burns

A

Includes whole surface area, skin becomes tourniquet (cannot expand because the skin is so tight. Treatment is escharotomy

124
Q

Local effects of burn injury

A

LOCAL EFFECTS = zone of the burn injury.

Each burn area has 3 zones of injury.

 Inner zone – area of coagulation – cellular death occurs – most damage sustained
 Middle zone – zone of stasis – compromised blood supply, inflammation & tissue injury
 Outer zone – zone of hyperaemia – sustains least damage

125
Q

Explain - Total Body Sureface area

TBSA%

A

TBSA 20% produce both a local & systemic response & considered major burn injuries

Burns

126
Q

SYSTEMIC EFFECTS of burns - Cardiovascular

A

Initial systemic effect is haemodynamic instability from loss of capillary integrity and shift of fluid, protein and sodium from the intravascular space into the interstitial spaces. Haemodynamic instability involves:

 Cardiovascular – Hypovolaemia,oxygen delivery = CO, BP. SNS releases catechlamines (adrenaline & noradrenaline) for vasoconstriction & ^HR. Fluid resus required, if not, distributive shock will occur

127
Q

SYSTEMIC EFFECTS of burns - respiratory

A

Inhalation injury – inhalation of noxious gas and superheated air (explosion or burning structure & trapped inside). Increases risk of pneumonia. Respiratory depression occurs in burns patients without evidence of smoke inhalation injury. Bronchoconstriction (due to release of histamine) and chest wall constriction secondary to circumferential full thickness chest burns causes respiratory depression. Hypoxia may occur (catecholamines released – vasoconstrictors) which hen requires supplemental oxygen. Intubation is required as soon as increasing airway obstruction is determined.

128
Q

SYSTEMIC EFFECTS of burns - Metabolic

A

Fluid & electrolyte alterations. During burn shock, serum sodium levels vary in response to fluid resuscitation. Usually hyponatraemia (sodium depletion) is present. Hyponatraemia is common during the first week of the acute phase as fluid shifts from the interstitial to vascular space. Immediately after burn injury, hyperkalaemia (excessive potassium) results from massive cell destruction. Hypokalaemia (potassium depletion) may occur later with fluid shifts and inadequate potassium replacement. Red blood cells destroyed results in anaemia. Blood transfusions required maintain adequate haemoglobin levels for oxygen delivery. Oedema occurs at the time of burn injury and is seen within 1 hour of injury when there is a fluid shift into the burn tissue. Patients with severe (>20%) burns develop massive systemic oedema. Reabsorption is dependent on the depth of injury to the tissue. As oedema increases this puts pressure on small blood vessels & nerves in distal extremities causing blood flow to be obstructed and consequent ischaemia. This is compartment syndrome. Escharotomy, surgical incision to the eschar (devitalised tissue from burn) to relieve the constricting effect of the burned tissue.

129
Q

SYSTEMIC EFFECTS of burns - Immunological

A

Immunological defences greatly altered by burn injury. Serious burns diminish resistance to infection. Sepsis remains one of the leading causes of death in burn patients. Loss of skin integrity is compounded by the release of abnormal inflammatory factors. These alterations result in immunosuppression and increase risk for sepsis. As a result, the major cause of death in the burn patient who survives after 24 hours is multiple organ dysfunction syndrome MODS. Infection controlled environment is important. Immunosuppression places burn patients at high risk of sepsis.

130
Q

Nursing intervention for burn care

A

Remove patient from danger – Stop the burning – Airway, look in mouth, look at tongue, up nose for signs of singed nose hair, cold running water or wet towels applied to burn area for 20 mins, remove clothing as they can continue to burn skin. Sedate & intubate if any signs of burns in nose or mouth as swelling will increase.

131
Q

Nursing care burns - Breathing

A

consider intubation & high flow oxygen (non-rebreather) as burns to the airway can cause swelling that blocks the flow of air into the lungs. Circulation, oxygen therapy, NIL by mouth to prevent aspiration of vomitus as nausea & vomiting occur due to paralytic ileus from stress of injury.

132
Q

Nursing care burns - Continuous vital signs monitoring

A

T, P, RR, BP, cardiac monitoring if history of cardiac disease, electrical injury or respiratory problems.
 Elevation of burned extremities to decrease oedema, elevation of lower & upper extremities on pillows or suspension using IV poles.
 Indwelling urinary catheter inserted for major burns to accurately monitor urine output and renal function.
 Tetanus prophylaxis administered if patients’ immunisation status is unknown because burns are contaminated wounds.
 Fluid resuscitation – management of fluid loss & shock – see below for calculation

133
Q

Burn injury management - Immediate care fluid resuscitation

A

Formula -

2mls/kgx %TBSA x Pre-body weight (In kg) = Volume in mls

134
Q

Fluid resus example:

A

Patient that was 60Kg pre-burn with 60% TBSA

(2mls/kg x %TBSA x pre-burn body weight (in kg) = volume in mls)

= 2ml x 60 %TBSA = 120

120 x 60 kg = 7200mls

135
Q

Fluid resus example breakdown:

A

50% of 7200 is required in the 1st 8 hrs post burn
= 3600ml

25% of 7200mls is required in the 2nd 8 hrs post burn
= 1800

25% of 7200mls is required in the 3rd 8 hrs post burn
= 1800

NOTE: on top of this fluid quantity, the pt will also require the β€˜normal’ daily intake of hydration over 24/24

Average intake = 200mls over 24/24 = 83mls
(2000 / 24)

  • In the 1st hour 533mls/hr of CSL
136
Q

Restoring normal fluid balance

A

monitor IV & oral fluid intake – Input, output & daily weights obtained to monitor fluid status changes.

137
Q

Preventing infection - burns

A

Clean technique used for wound care procedures – provide a safe & clean environment & check burn wound to detect early signs of infection

138
Q

Maintaining adequate nutrition

A

when bowel sounds resume oral fluids should be initiated slowly – patient’s tolerance noted & fluids increased gradually and normal diet resumed if vomiting & distension do not occur. Nurse to liase with dietician to plan a diet acceptable to the patient

139
Q

Promoting skin integrity - burns

A

Support patient during emotionally, distressing & painful experience of wound care. Nurse to make assessments of the wound status & record changes or progress in wound healing and keep all members of the healthcare team informed of changes in the wound or treatment.

140
Q

Fluid resus example breakdown:

A

50% of 7200 is required in the 1st 8 hrs post burn
= 3600ml

25% of 7200mls is required in the 2nd 8 hrs post burn
= 1800

25% of 7200mls is required in the 3rd 8 hrs post burn
= 1800

NOTE: on top of this fluid quantity, the pt will also require the β€˜normal’ daily intake of hydration over 24/24

Average intake = 200mls over 24/24 = 83mls
(2000 / 24)

  • In the 1st hour 533mls/hr of CSL

Need to prevent over loading, hence the 24 hour period

Normal daily intake 2000ml over 24 hour = 83ml
50%
25% = 83ml each
25%

141
Q

Promoting physical mobility - burns

A

Priority to prevent complications from immobility. Deep breathing, turning, proper repositioning are essential to prevent atelectasis, pneumonia, & prevent ulcers & contractures. Early sitting & ambulation are encouraged. Prevention of DVT, compression bandages in lower limb burns promote venous return & minimise oedema formation.

142
Q

Strengthening coping strategies - burns

A

Depression, regression & manipulative behaviours are common responses of patients who have burn injuries. Psychological distress & depression are common in people who have experienced burns. Nurses can assist patients to develop effective coping strategies by setting specific expectations for behaviour, build trust, give positive reinforcement when appropriate.

143
Q

Supporting patient & family processes - burns

A

Family functioning is disrupted with burn injury. Nurses responsibility is to support the patient & family & to address their spoken & unspoken concerns. Family members need to be instructed about ways that they can support the patient as adaptation to burn trauma occurs. Burn injuries impacts patient & family psychologically, economically & practically. Social support & counselling should be made available. Patient & family education. Assess learning styles of patient & family & tailor teaching activities to these.

144
Q

Monitoring and managing potential complications - burns

A

Heart failure & pulmonary oedema – acute respiratory failure & acute respiratory distress syndrome – visceral damage

145
Q

Rehabilitation Phase – from major wound closure to return to individual’s optimal level of physical and psychosocial adjustment - burns

A

 Psychological support

 Abnormal wound healing

146
Q

Discuss emergency procedures at the burn scene

A

 Extinguish the flames – smother flames – stop, drop, roll – disconnect electrical source if burn source is electrical
 Cool the burn – tepid running tap water for 20 mins or cool wet towels – NO ICE
 Remove restrictive objects/clothing
 Cover the wound – use cling film as it is sterile – minimises bacterial contamination – decreases pain by preventing air coming into contact with the burn – no creams or ointments at they compromise the assessment of the burn
 Irrigate chemical burns – if at home brush off the chemical agent, remove clothing immediately, rinse all areas of the body that have come into contact with the chemical with running water/shower.
 Local effects of a burn are most evident but the systemic effects pose greater threat to life. Primary survey ABC, C spine, cardiac monitoring for patients with high voltage electrical injuries.

147
Q

%TBSA fluid resus example

A

2ml x 80kg x 25% TBSA + 2000ml

A 80kg pt has 25% TBSA burn. The pt is NBM so include the 2L maintenance fluid requirements.

Formula:
2ml x kg x %TBSA + 2oooml
=

6000ml

148
Q

The incidence of burns in AUST/NZ 1999 - 2004 is?

a) 460 admissions
b) 4,600 admissions
c) 46,000 admissions

A

Answer = C

149
Q

The Classification of burns injuries is superficial, partial thickness and full thickness

True / False

150
Q

Complete the following statement

We use the rule of nines TBSA% to ………

A

Calculate how much is burnt & how much we need to fluid resus

151
Q

Name three local effects of a burn

A
  1. Inner zone:
    - area of coagulation
    - cellular death occurs
    - most damage sustained
  2. Middle zone:
    - Compromised blood supply
    - inflammation
    - tissue damage
  3. Outer zone:
    - Zone of hyperaemia (excess of blood in the vessels)
    - Sustains least injury
152
Q

Name three systemic effects of a burn

A
  1. Cardiovascular:
    - hypovolemia
  2. Respiratory:
    - Bronchconstriction
  3. Metabolic:
    - hyponatraemia (
153
Q

At risk groups

A

– elderly & infants

154
Q

Paeds Considerations

A
  • Are more at risk of heat loss and fluid loss due to increased surface area to volume ratio
  • > risk of dehydration & hypothermia
  • > risk of hypoglycaemia due to metabolic rate (b/c they’re continually developing
  • Any fluid requirement needs to be calculated by weight
  • Adjust 02 delivery
  • ABGs & electrolyte values are the same as adults
155
Q

Paeds airway

A
  • Different from adult
  • Large tongue, short trachea
  • Newborn larynx is 1 3rd of adults
  • Do NOT do head tilt, neck it too short = occlude airway
  • Keep in neutral nose up position
  • Risk for aspiration is high
156
Q

Paeds breathing

A
  • RR = 40 bpm
  • Underdeveloped intercostal / accessory muscles
  • Tachypnoea is a normal response
  • Slowing RR (is not an improvement) could mean impending collapse (decompensating)
  • RNs do NOT do nasopharyngeal on infants (nasal breathers) need advanced nurse
157
Q

Paeds 02 therapy

A
  • Nasal prongs, CPAP, BiPAP, head box, adults masks if emergency
  • Head box is better – the infant can still see shadows etc.… & parents can see child
158
Q

Paeds Airway / Breathing assessment

A
  • Ensure patency
  • Good to hear the infant cry = clear airway
  • Assess for adventitious sounds – stridor, wheeze, grunting
  • Resp distress = head bobbing, nasal flaring, intercostal or sternal recession
  • Fatigued / flat child – NOT good
159
Q

Paeds airway/breathing conditions - Croup

A
  • Acute swelling causing upper airway obstruction
  • Treat with steroids and
    nebulised adrenaline
160
Q

Paeds airway/breathing conditions - Epiglottitis

A
  • Inflammation of the epiglottis

- urgent intubation, nurse upright/supoorted until EET

161
Q

Paeds airway/breathing conditions - Foreign body aspiration

A
  • anything small enough to fit in the mouth

- coughing, back blows, removal of FB with magill forceps

162
Q

Paeds airway/breathing conditions - Broncholitis

A
  • viral - obstruction of small airways resulting in air trapping
  • Continuous monitoring, SP02 - supportive management
163
Q

Paeds airway/breathing conditions - asthma

A
  • mucosal and immune system dysfunction - lower resp
    inflammation of the airways
  • asthma severity assessment, oxygenation, bronchdilation, steroids, magnesium
164
Q

The Ventilated Infant/Child

A 
ETT uncuffed up to puberty, the tube is monitored very closely, 
Suctioning, 2-6hlry , suction catheter less than 2/3 the internal diameter of the ETT
Humidification necessary
Gastric Decompression
Restraints required
Analgesia and sedation 
Ventilator
Non invasive vent
Bi PAP, CPAP
High frequency oscillatory ventilation
165
Q

Paeds Circulation

A 
Pulses
Brachial
BP – Age related (p888)
Fluid and drugs calculated on weight
Urine output 0.5-2mls per hour
Calculating child's weight
(Age + 4) x 2
Broselow Tape
166
Q

Paeds - Circulation Physiology and pathophysiology

A

Children compensate for hypovolaemia by vasoconstriction and tachycardia, and may lose up to 30% of blood volume before becoming hypotensive
The pulse pressure will narrow before hypotension occurs.
Capillary refill is a non-specific sign of circulatory compromise in a hypothermic child.
Tachycardia is also non-specific, and occurs in children who are hypovolaemic, in pain, frightened, hypoxic, hypercapneic, having seizures etc. Look for the cause and treat it.

167
Q

Fluid Maintenance in Paediatrics

A 
Patients weight:
3kg - 10kg
Mls/day:
100mls x weight
mls/hour:
4 x weight

Patients weight:
10kg - 20kg
mls/day:
1000 plus 50 x (wt - 10)
mls/hour:
40 plus 2 x (wt - 10)

Patients weight:
> 20kg
mls/day:
1500 plus 20 x (wt - 20)
mls/hour
60 plus 1 x (wt - 20)

IV fluids are different and commonly used fluids are 0.45% Normal Saline and 2.5%

168
Q

Paeds shock:

hypovolemic

A

Commonest form of shock in children, HR not BP
Haemorrhage, trauma, GIT bleeding, burns, peritonitis & diarrhoea.
Responds well to fluid resuscitation
Fluids titrated to maintain adequate cardiovascular function

169
Q

Paeds: Septic shock

A

Manifests as hypoxemia, hyperthermia or hypothermic, HR, cap refill, peripheral pulses, cool, mottled, urine output.

170
Q

Management of paeds shock

A

Assessment ABCDE (rash)
Cardio respiratory monitoring, temperature, urine output, ABG, U&E
Fluid resuscitation, early and aggressive, within first hour, before hypotension develops, O2 therapy
Improve cardiac performance, optimise O2 delivery to tissues
Inotrope/vasopressors (dopamine, dobutamine/adrenaline and noradrenaline)

171
Q

Paediatric Anatomy & Physiology differences

A 
Gastrointestinal system
Central nervous system
Cardiovascular system
Respiratory system
Integumentary system
Musculoskeletal system
172
Q

Paeds: Disability

A 
Neurological Dysfunction 
Meningitis
Encephalitis
Seizures
Encephalopathy
173
Q

Paeds Trauma

A

MVA’s
trauma
near drowning
assault & falls

Similar to adults, trauma team

174
Q

Older Adult

A

Adults older than 65 use 46% acute care beds although only 12.5% of the population
Most common admissions include Arrhythmias, heart failure, stroke, fluid and electrolyte imbalances, pneumonia, hip fractures

175
Q

The older adult in critical care

A

Multi-system conditions and co-morbidities
Arrhythmias, heart failure, stroke, fluid and electrolyte imbalances, pneumonia, hip fractures
Identify falls risk, early d/c and assistance required, interdisciplinary teams, community based referrals, standard protocols

176
Q

Older adult considerations

A

Surgical risk- higher so ICU or HDU admissions
Delirium, sensitive to changes in fluids,
metabolic and nutritional imbalances,
medications and infections
Nosocomial infections, decreased immuno- competence, underlying disease, increased drug adverse reactions

Pain management
Medication use poly-pharmacology,
Depression
Nutrition, physical and social considerations

177
Q

Age related changes and associated clinical manifestations

A

Cardiovascular, cardiac output, rate and rhythm, structural changes, arterial circulation, venous circulation, peripheral pulses
Respiratory, structures, ventilation and perfusion, ventilation control, lung compliance decreased
Urinary- bladder- functioning nephrons decreased, excretion of toxins decreased

178
Q

Intensive Care

A 
Patients may require Intensive care for any of the following:
Instability (hypotension/hypertension)
Respiratory compromise
Cardiac arrhythmias
Acute renal failure
Multiple organ failure
Intensive invasive monitoring
Post surgery
179
Q

Structure and Function of the Abdomen

A 
Surface landmarks
Borders of abdominal cavity
Abdominal muscles
Internal anatomy (viscera)
Solid viscera
Liver
Pancreas
Spleen
Adrenal glands
Kidneys
Ovaries
Uterus
180
Q

Solid viscera:

A
  • Liver - bleed a lot in trauma – total body fluid requirements
  • Pancreas
  • spleen - bleed a lot in trauma – total body fluid requirements
  • adrenal glands
  • kidneys
  • ovaries
  • uterus
181
Q

Hallow viscera:

A
  • stomach
  • gallbladder
  • small intestines
  • colon
  • bladder
182
Q

Referred pain

A

cardiac, gallbladder, kidneys etc.

183
Q

Flank pain – Kidneys / UTI

A

Refers to discomfort in your upper abdomen or back and sides
It develops in the area below the ribs and above the pelvis. Usually, the pain is worse on one side of your body.
Most people experience flank pain at least once in their life, and the discomfort is usually temporary.

184
Q

Referred Shoulder Pain

A

laparoscopy, ectopic pregnancy

185
Q

Incidence of cancer

A
  1. Prostate 2. Bowel 3. Breast 4. Melanoma 5. Lung
186
Q

Acute renal failure (ARF):

A
  • 20 – 25% of all ICU patients

* > mortality rate

187
Q

Chronic Kidney disease (CKD):

A
  • More common I women

* Diabetic patients – 35% over 20 years has it

188
Q

The Nephron:

A

Each kidney has approx. 1 million nephrons

189
Q

Abdominal wall divided into four quadrants

A 
Right upper (RUQ)
Left upper (LUQ)
Right lower (RLQ)
Left lower (LLQ
190
Q

Special Procedures for Advanced Practice

A

Rebound tenderness (Blumberg’s sign), choose a site away from tender area, pain on release of pressure
Inspiratory arrest (Murphy’s sign), inflamed gall bladder, pain on deep breath when palpating liver
Iliopsoas muscle test, ? Appendix/leg lift
Obturator test, questionable

191
Q

Causes of Abdominal Complications

A 
Infections
Trauma (blunt and Penetrating)
Inflammation
Pre-existing conditions
Cancers
Organ failure
192
Q

Renal Failure

A 
Acute Renal Failure (ACR)
20-25% of Intensive Care patients
High mortality rates 
Poor outcome if RRT required
Chronic Kidney Disease
CKD is more common among women than men.
More than 35% of people aged 20 years or older with diabetes have CKD.
More than 20% of people aged 20 years or older with hypertension have CKD
193
Q

The Nephron

A 
Each Kidney has approx 1 million nephrons
Filters blood to produce urine
Each nephron contains
Glomerulus
Glomerulus (Bowmans) capsule
Loop of Henle
194
Q

RENAL FAILURE – Pre-renal

A 
Pre-renal
Blood supply to the kidneys 
	hypovolemia
	decreased cardiac function
	decreased peripheral vascular disease
	decreased renovascular blood flow
195
Q

Renal Failure – Intra renal

A

Acute Tubular Neurosis (ATN)
Glomerulonephritis
Nephrotoxicity
Vascular insufficiency

196
Q

Acute tubular neurosis (ATN)

A

Damage to the tubular portion of the nephron may be caused by more than one mechanism.
Most commonly associated with administration of nephrotoxic agents in association with prolonged hypoperfusion or ischemia.
Provoked by Infection , blood transfusion, drugs, ingested toxins and poisons complication of heart failure or cardiovascular surgery.
Term often used in ICU to describe ARF. Accounts for 30% ARF in ICU.

197
Q

Glomerulonephritis

A

Infective/inflammatory process damaging glomerular membrane or a systematic autoimmune illness attacking the membrane. This allows larger blood components eg plasma proteins and WBC cross the membrane. This causes tubular congestion and nephron failure.

198
Q

Nephrotoxicity

A 
Damage to nephron from causative agent
Drugs
Antibiotics
anti-inflammatory
cancer drugs
radio opaque dies.
199
Q

Vascular Insufficiency

A

1/3 of pts in ICU have chronic renal dysfunction.
May be undiagnosed related to diabetes, ageing process , hypertension.
These factors create reduction in vasculature of the kidney therefore reduce glomerular filtration.

200
Q

RENAL FAILURE – Post renal

A 
Benign prostatic hyperplasia
Bladder cancer
Calculi formation
Neuromuscular disorders
Spinal cord disease
Strictures
Trauma (back, pelvis, perineum)
201
Q

Acute renal failure

A

Clinical history essential in differentiating between pre-existing renal disease and potential for ARF
Clinical History along with key assessments allow for accurate diagnosis

202
Q

RIFLE Criteria for ARF

A 
Assessment 
renal output, 
serum creatinine levels, 
HR, 
CVP, 
BP, 
PCWP
203
Q

Clinical Management - renal

A 
Reducing further Damage
IV fluid resuscitation
Assessment for renal outflow obstruction
Cease or modify any nephrotoxic drugs or agents  
Treat infection with alternate less toxic antibiotics
Nutrition
Enteral or Parenternal
30-35kcal/kg/day
Protein intake 1-2g/kg/day
Renal replacement Therapy (RRT)
204
Q

MANAGEMENT OF ARF

A

If conservative measurements fail, renal replacement therapy is required to:
Control blood biochemistry
Prevent toxin accumulation
Allow removal of fluids to allow adequate nutrition
One criteria is sufficient to initiate RRT
Two or more signify urgent and mandatory RRT

Renal replacement therapy Initiation criteria (Box 18.1, Elliott et al 2015 p 595)
Oliguria (UO  6.5mmol/L)
Severe acideamia (pH 30mmol/L)
Clinically significant organ (esp Lung) oedema
Uraemic encephalopathy
Uraemic pericarditis
Uraemic neuropathy/myopathy
Severe dysnatreamia (Na > 160 or
205
Q

Renal therapy options

A 
Peritoneal dialysis
Haemodialysis 
Continuous renal replacement therapy (Acute) 
Haemodialysis Community based (Chronic) 
Access - Catheter 
AV access
AV fistula – (no catheter)
Renal transplant
206
Q

Liver failure

A

Liver failureis the inability of theliverto perform its normal synthetic and metabolic function as part of normal physiology.
There are two types of liver failure
Acute
Chronic

207
Q

Acute Liver Failure

A

Acute Liver Failure is the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver disease
Diagnosis
Based on:
physical exam
laboratory findings
patient history
past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence of known prior liver disease respectively

208
Q

Chronic Liver Failure

A

Usually associated with Cirrhosis & can develop from viral Hep B & C, alcohol, metabolic (Wilson’s disease) or autoimmune.

209
Q

Consequences of Liver Failure

A 
Hepatic Encephalopathy
Hepatorenal Syndrome
Varices & Variceal Bleeding
Ascites
Respiratory Compromise
210
Q

Liver Transplantation

A

Orthotopic Liver Transplantation
Split-liver Transplantation
Adult-Living Donor Transplantation

211
Q

Liver - Clinical Deterioration

A

Failure to Rescue
Specified MET criteria for health care facilities
Parameters set for notification for specific patients
National consensus statement: essential elements for recognising and responding to clinical deterioration (Australian Commission on Safety and Quality in HealthCare)

212
Q

The kidneys…

A

Filtration
Reabsorption
Secretion

213
Q

Multiple Organ Dysfunction Syndrome (MODS)

A

 Closely related to outcome of Sepsis
 Abnormal cellular responses involving multiple organ systems
 Sequential process – flows – domino effect – teying to treat & prevent at the same time
 Complex Process
 Simultaneously involving every cell type

214
Q

Pathophysiology of MODS

A

 Hypoxic - Hypoxia is caused by altered metabolic regulation of tissue oxygenation starving tissue
 Microcirculatory injury occurs – damage & injury to micro vessels – kidneys, lungs, brain etc.
 During Sepsis or ischemia mitochondria cause cell death rather than restore homeostasis
 Can happen over several days 4,5,6,7 days eg. Burns patients

215
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

 SIRS
β—¦ Inflammatory state affecting the whole body
β—¦ Serious condition related to systemic inflammation, organ dysfunction & organ failure
β—¦ Abnormal regulation of cytokines
β—¦ Signs and symptoms
 SIRS > Sepsis > Shock > MODS
 Wide spread inflammation: heart, kidneys etc… kidney fails = domino effect = MODS

216
Q

Signs and Symptoms of SIRS

A

 Systemic inflammatory response syndrome must be diagnosed by finding at least any two of the following:
 Temperature 38.5 degrees – hypo or hyperthermia
 Heart Rate >90 - tachycardia
 Tachypnoea RR >20
 WCC – significantly low or elevated – white cell count
 Second, SEPSIS = other comorbidities
 Third, signs of end-organ dysfunction
 * must be diagnosed with at LEAST two symptoms

217
Q

Treatment of SIRS

A

 Treatment primarily consists of the following:
β—¦ Volume resuscitation
β—¦ Early antibiotic administration
β—¦ Early goal directed therapy - is individual to patients needs
β—¦ Rapid source identification and control – what caused it? Where did it start? Eg. Did they get pancreatitis pre or post-surgery
β—¦ Support of major organ dysfunction

218
Q

Organ Dysfunction

A

 Early identification of organ dysfunction critical
 Early intervention reduces damage > recovery –
Car analogy- flat tyre – get it changed & fixed = short recovery time
If you keep driving on it – will damage the rim, road, driveway = will need to fix all of them
= long recovery time
 Risk of death 11-23% as each organ fails
 Up to 75% of patients in sepsis have at least 2 failing organs
 Organ failure cascade:
ο‚– Pulmonary system
ο‚– Cardiovascular
ο‚– Renal
ο‚– Haematological system

219
Q

Thrombotic Microangiopathy (TMA)

A

 Formation of microvascular platelet aggregates (and possible fibrin formation)
 Meaning – clots develop in the macrovascular area
 Usually caused by injury to microvascular endothelium:
β—¦ Haemolytic anaemia, > liver enzymes,

220
Q

Disseminated intravascular Coagulation (DIC

A

 Widespread activation of tissue factor –dependent coagulation (

221
Q

Neurological Dysfunction

A

 MODS can result from:
β—¦ Traumatic brain injury - CVA
β—¦ Subarachnoid haemorrhage – SPONTANEOUS BLEED
 Causes respiratory and cardiovascular organ dysfunction
 Due to dysfunction of the sympathetic nervous system
 Survivors of sepsis induced MODS may suffer cognitive impairment

222
Q

Measuring organ dysfunction

A

 Many scoring systems for predicting mortality
 Some adapted for assessing organ dysfunction
β—¦ APACHE (acute physiology and chronic health evaluation)
β—¦ SAPS (simplified acute physiology score)
β—¦ MPM (mortality probability models)
 Specific organ dysfunction assessments
β—¦ SOFA (Sepsis-related/sequential organ failure assessment

223
Q

SOFA (Sepsis-related/sequential organ failure assessment)

A 
	Uses the worst values for 6 clinical parameters within 24hr period:
β—¦	Pa02/Fi02
β—¦	Platelet count
β—¦	Bilirubin
β—¦	BP
β—¦	GCS
β—¦	Urine output/creatinine concentration
	As number of dysfunctional organs increase – SOFA score increases – mortality increases
224
Q

MODS Survival

A 
	Shock Management
	Awareness of Secondary Insults – what could go wrong 
	High level critical care management
	Prevention and management
β—¦	Effective shock resuscitation
β—¦	Timely treatment of infection
β—¦	Exclusion of secondary inflammatory insults
β—¦	Organ support
225
Q

Appropriate Interventions

A

 Interventions to reduce MODS from Sepsis
β—¦ Surviving sepsis guidelines (SSG)
ο‚– Based on clinical evidence
ο‚– Graded according to the quality of evidence
β—¦ Early Goal Direct Therapy (EGTP)
ο‚– Provides clinicians with target outcomes for treatment in early sepsis management
ο‚– Encourages early intervention

226
Q

Early treatment of Infection / MODS

A

 Essential in Prevention and Management of MODS
 Antimicrobial therapy in septic shock essential
 Inappropriate initial antimicrobial therapy = five fold decrease in survival
 Increase in incidence of acute kidney injury if antimicrobial therapy delayed
 Treat early!

227
Q

Further consideration - MODS

A

 MODS is complex and requires highly skilled nurses
 Understanding of pathophysiology, inflammatory response and sepsis essential if early intervention is to be implemented
 Nurses require:
β—¦ High knowledge base
β—¦ Vigilant assessment skills
β—¦ Identification of interventions required
β—¦ Prioritisation skills
β—¦ Time management skills

228
Q

Critical care

A

 117,000 ICU attendances per year in Australia
 Survival rate of 89% that reach discharge
 >6 months for functional recovery at home -
 Physical deconditioning
 Neuromuscular dysfunction
 Psychological issues

229
Q

Burden of Critical Illness

A

When the patient leaves the ward, their journey is just beginning….
The longest part of recovery
We need to supply them with all the resources & referrals

230
Q

Change of practice – need to have a holistic perspective - critical care

A

 Critical care one component in the continuum of care
 Critical illness begins with onset of acute illness, includes ICU and incorporates the risk of related problems
 Nurses now consider patients recovery in terms of:
 Health Related Quality Of Life (HRQOL)
 Need to continue the concept of holistic care beyond the ICU

231
Q

Holistic critical care

A 
Primary Survey 
	A - Airway 
	B - Breathing
	C - Circulation
	D - Disability
	E – Exposure
232
Q

Continuing Care - secondary survey/critical care

A

 A – Awaken the Patient Daily
 B – Breathing trials (to minimise mechanical ventilation duration)
 C – Coordination (to daily awaken and spontaneous breathing trials)
 D – Delirium Monitoring
 E – Exercise/Early Mobility (requires a patient to be

233
Q

Problem with ICU admission

A

 46% of Patients acquire ICU Acquired Weakness (ICU-AW)
 Critical illness Myopathy
 Polyneuropothy – nerves weakness to multiple nerves
 Neuromyopathy – muscle
 Acquisition of ICU-AW is associated with:
 Co-existing conditions (COPD, CCF, DM)
 Critical Illness (Sepsis, SIRS)
Treatments (mechanical ventilation, hyperglycaemia, sedatives, immobility

234
Q

HRQOL – Health related quality of life

A

 Measurements need to be taken to ensure the patient meets HRQOL indicators
 Patients must be considered holistically
 Measurements taken to ensure appropriate development in:
 Physical Function
 Psychological function
(See pg 60 Elliott 2012 for measurement tools)

235
Q

Psychological effects of ICU (worse than physical)

A 
	Physical recovery can be short
	Psychological recovery can be long
	Effected by memories and experiences
	Patients suffer
	Powerlessness
	Reality-unreality
	Reactions and acceptance
	Comfort-discomfort
	Anxiety
	Depression
	PTSD

Comes out over time, the patient may have been a very fit & active person – accident occurs – wake up in ICU 3 weeks later….

236
Q

Psychological Care - critical care

A

 Psychological care of post ICU patients can be difficult
 Long term
 Specific interventions
 Patient diaries – provides missing pieces of information
 Not all patients want to be reminded of their experience
 Regular psychological assessment recommended by NICE
 Including 2-3 months after being at home/rehab

237
Q

Recovery at home - critical care

A 
	5% of patients who survive will die within 12 months
	Follow up essential
	ICU FU Clinics       - - follow up clinics 
	Review progress
	Identify problems early
	Coordinate care
	Support rehab
	Discuss ICU experience
	Offer visits to ICU
	Allow relatives to ask questions
238
Q

REMEMBER!

A

 Remember – discharge begins at admission
 Planning of care needs to be long term
 Considerations at home
 Care needs to be Holistic

A –E assessment
Realistic goals
Do they need any help / other services to help at home?

239
Q

THE END

A

Good luck, work your socks off
& you’ll get where you want to be
X

NUR 305 Sam Fox (1 decks)

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