Wk 1: Respiratory Flashcards
1
Q
Define ventilation
A
the movement of air between the atmosphere and the lungs. Inspiration and expiration.
2
Q
Define diffusion
A
the exchange of oxygen and carbon dioxide between the bloods red blood cells and the lungs.
3
Q
Define perfusion
A
delivery of RBCs to the lungs
4
Q
Define compliance
A
indication of how well the chest wall and lungs can expand and collapse. If the patient has decreased compliance, it is more difficult to inflate the lungs.
5
Q
Define resistance in the context of airways
A
This relates to the size of the airway. The resistance of the airway increases when the diameter of the airway decreases.
6
Q
Define V/Q mismatch
A
When there are issues with ventilation and perfusion, the diffusion of gases is altered. This is called a V/Q mismatch
(ventilation/perfusion)
7
Q
What smaller systems become compromised in the context of APO?
A
Our lungs are kept dry by
- Lymphatic drainage
- Hydrostatic pressure (pressure exerted by fluid in vessel)
- Capillary oncotic pressure (pressure exerted by proteins, keeps fluid in the capillaries)
- Capillary permeability
- Presence of surfactant (repels water, stops fluid entering alveoli)
8
Q
What does a disruption in the ‘drying’ system of the lungs cause in APO?
A
- abnormal accumulation of fluid on the lungs in the interstitial tissue and alveoli of the lungs.
9
Q
What complication arrises from the build-up of fluid in APO?
A
- impaired gas exchange
- impaired lung expansion
10
Q
What is the cause of cardiogenic APO?
A
- heart failure
11
Q
Recall, what is heart failure?
A
Multiple processes that result from either;
- impaired left ventricular contraction (systolic heart failure)
- impaired left ventricular relaxation (Diastolic)
When it cant flow out into the body it backs up in the pulmonary veins and then into the lungs thus causing fluid not being able to move into the blood.
12
Q
Explain the pathophysiology of cardiogenic APO
A
- When the heart is failing to meet the demands of the blood flow.
- as the pressures in the heart increase-> cardiac output (CO) is decreased, as the ventricle must pump against an increased systemic vascular resistance (SVR).
13
Q
What pathophysiological processes are causes of cardiogenic APO?
A
- Blood returning to left atrium exceeds that leaving the left ventricle
- This results in an increased pulmonary venous pressure
- This then causes an increased pulmonary capillary hydrostatic pressure. As the hydrostatic pressure increases and exceeds the pulmonary oncotic pressure, there is a net filtration of protein-poor fluid out of the capillaries and into the interstitial spaces and alveoli.
14
Q
What are some common cardiac-related causes of APO?
A
- heart disease/left ventricle dysfunction
- AMI
- acute dysrhythmia
- Valvular insuffucuency
- fluid overload
15
Q
What are some common non-cardiac related causes of APO?
A
- capillary injury
- increased capillary pressure
- redistribution of blood volumes or flow to lungs as a result of patient positioning, administration of vasoactive drugs, cardiac shunts, anemia or exercise
- increased IV volume from over transfusion of fluids or renal failure - physical injury affecting pulmonary parenchyma (where gas exchange occurs)
- reduced drainage from interstitial space as a result of blood contents including electrolytes and plasma proteins creating an osmotic pressure that draws water from the IS to IV space.
- obstruction of the lymphatic system
- blood transfusion/fluid overload
- acute lung injury
- high altitude
- tissue injury due to toxicity
- tissue injury due to damaging pressure
- Common examples include pneumonia, aspiration of gastric contents, sepsis, thoracic surgery and large-volume blood transfusion.
- pulmonary contusion, inhalation of noxious substances and burns
- High-altitude pulmonary oedema is caused by cellular injury induced by pulmonary hypertension secondary to altitude-induced hypoxia.
- reduced drainage of the interstitial space
- neural and hormonal responses to cerebral lesions and head injuries
- left ventricular failure or mitral valve disease causing pulmonary venous pressure that increases pulmonary capillary pressure.
- In left ventricular failure, the ability of the heart to pump blood is impaired and this causes blood to back up into the pulmonary vasculature, leading to an increase in pulmonary capillary pressure. - inadequate CO results in peripgeral vaso constriction to bring blood bacll to the core orans which furthers the problem of pressures and furthers the leaking of fluid out of IV space due to the great hydrostatic pressure.
- Common causes of left ventricular failure include coronary artery disease, myocardial infarction, cardiomyopathies and excessive workload of the heart caused by hypertension, arrhythmias
(including atrial fibrillation) or valve disease
16
Q
What are some clinical manifestations of APO?
A
- Sudden onset of extreme breathlessness/dysponoea
- particular dyspnoa when lying down.
- Tachypnoea
- Chest auscultation – crackles and rattles
- O2 desat
- Cough
- altered concious state
- Pink frothy sputum present if alveoli injured
- Cyanosis (late sign)
- Tachycardia
- Hypertension (because of hyper-adrenergic state)
- cardiac arrhythmias (e.g. A fib considering its high in heart failure)
- Hypotension = severe LVF and cardiogenic shock
- Diaphoresis
- Raised JVP
- Anxiety and agitation
- Confusion
- pink
(blood tinged) frothy sputum in late stages
17
Q
What are some important considerations we must make when looking at one’s clinical manifestations in the context of APO?
A
= Think about why the pat would be experiencing these and link it to the pathophysiology.
For example, why would the patient develop tachycardia? Well, the patient who is experiencing cardiogenic APO has a failing left ventricle. The left ventricle is unable to pump effectively and eject blood forwards (into the aorta). This means that the patient has a reduction in their cardiac output (CO). If you think back to the equation cardiac output = stroke volume x heart rate (CO = SV x HR). So the patient will increase their HR as a way of increasing their cardiac output.
18
Q
What are the common precipitating factors of APO?
A
- acute coronary syndrome
- new onset arrhythmia
- post surgery complications
19
Q
Nursing management of APO
A
- multidisciplinary approach
- excellent communication
- pt and family reassurance in acute exacerbations as can be very frightening.
- accurate assessment, management and evaluation.
- continued evaluation post intervention
- continued assessment with acknowedgement of ow quickly deterioration can occur.
20
Q
Explain the pathophysiology of general APO
A
- the amount of fluid in
the interstitial space increases, and the alveoli start to flood causing life-threatening impairment of gas exchange. - At its most extreme, the excess fluid causes ‘froth’ to form in the
lungs that blocks the airway
21
Q
What are the four pathophysiological phases that occur in APO?
A
1: increase in interstitial fluid, but without fluid flooding the alveoli.
- The lymphatic system becomes distended as it fails to
completely drain excess fluid.
- Pressure on the capillaries can cause narrowing; however, overall alveolar function is maintained and the only clinical sign is mild dyspnoea.
- The lungs are distensible and are able to handle considerable volumes of fluid before gas exchange is affected.
- However, increasing pulmonary oedema reduces overall lung compliance.
2. fluid starts to infiltrate the alveoli, but gas exchange remains adequate.
- At this point, it is possible to detect clinical signs of oedema on chest radiography
3. clinical signs become more apparent where gas exchange becomes compromised further. Oxygenation is affected, though adequate removal of carbon dioxide may be maintained. On chest auscultation, rales are heard on inspiration and chest radiography shows opacity of the lungs.
4. flooding of the alveoli is extensive, pink frothy sputum is produced and this stage is likely to be fatal without treatment. The aetiology of pulmonary oedema is related to alterations in capillary pressure, osmotic pressure, airway pressure or alveolar-capillary membrane integrity.
22
Q
What is the goal of treatment in APO?
A
- treat the underlying cause
- mitigate hypoxia
- mitiage fluid in lungs
23
Q
What is the nursing management for APO: Airways?
A
- suctions
- focus on breathing management
24
Q
What is the nursing management for APO: Breathing?
A
- consider position changes such as sitting up or standing (re-distribution of blood volume to peripheries takes load of heart)
- high flow via non-rebreather O2 (if below 90%)
*Oxygen is a powerful vasoconstrictor, and for patients for whom myocardial infarction is their primary event, this may worsen their prognosis. - NIPPV (CPAP or BiPAP)
25
What is included in your respiratory assessment?
Inspections
- peripheral and centeral cyanosis
- resp rate
- WOB
- O2 sats
Palpation
Auscultate
- note the presence of adverse noises and the level to which breath sounds extend.
- arterial blood gas (assess oxygenation and acid-base thus guide treatment)
- chest X-ray (show presence of pulmonary congestion)
Percussion
26
What focused assessments should be considered when suspected APO and why?
1. Respiratory
- get a clearer picture of what is going on.
2. Cardiac
- as some symptoms including breathlessness are associated with MCI so must be counted out.
27
What does NIPT do for those with APO?
- reduce risk of endotrachael intubation
- improves gaseous exchange as increases O2 avalible
- optimises lung volumes
- reduces the WOB as reduces the force needed to initiate each breath.
- increases functional residual capacity and thus improves lung compliance
- positive intrathoracic pressure also decreases preload and left ventricular afterload as it is harder for blood to re-enter this area of the body.
* must consider hypotension as a side effect as low venous return to the heart.
28
What is the nursing management for APO: circulation?
- Manual pulse check to assess rhythm
- manage pain and recheck. often chest pain
- assess skin for cool clamy extremities indicating hypoperfusion
- 12 lead ECG may provide info on underlying cause
- IV pathology as per below
- take bloods for renal function (urea and creatinine), FBC, BGL and troponin.
- ?blood cultures if suspected infection
- FBC to monitor for renal perfusion
- ?need for catheter (consider insertion and how lying flat may impact them)
29
What are the two first-line medications for patients with APO?
- vasodilators e.g. GTN
* contraindicated in pts with aortic stenosis
- diuretics e.g. fresuomide
30
What is the nursing management for APO: Disability?
- acute distress is common so reassurance
- check GCS frequently
- IDC
- BGL
- opioids can assist with this distress. Morphine for example is known as a mild vasodilator thus helping with pressure on heart.
- monitor AVPU in relation to hypoxic delirium
- check BGL (undiagnosed diabetes in common in heart failure patients)
31
What is the nursing management for APO: Exposure?
- check for signs of peripheral odema
- check core and peripheral temps
- Look out for a pattern of orthopnoea or a history of paroxysmal nocturnal dyspnoea where
a patient may describe waking suddenly feeling extremely breathless
32
Describe what the long term management of non-cardiogenic APO may be?
- discharging patients into a structured self-management plan is the best way to improve their long-term prognosis.
- GP check-up 1/52 post d/c
33
Describe what the long term management of cardiogenic APO may be?
- follow up with cardiologist or a specialist heart failure team within two weeks.
34
What dictates the autonomic nervous system's control over our ventilation?
- Receptor in muscles and joints
- central chemoreceptors
- peripheral chemoreceptors in arteries
- other receptors (e.g. pain and emptional stimuli acting through the hypothalamus)
- higher brain centers (cerebral cortex-voluntary control over breathing)
These all impact the resp center (medulla and pons) and dictate stretch receptors in lungs and irritant receptors.
35
How does APO affect the body; neurologically?
- hypoxia may cause confusion or agitation
36
How does APO affect the body; cardiac?
- Left ventricular failure, the ability of the heart to pump blood is impaired and causes blood to back u into the pulmonary vasculature resulting in an increase is pulmonary capillary pressure.
- the body's response to the inadequate blood flow is vasoconstriction which further exacerbates the pressure in the pulmonary capillaries and causes fluid to leak into the tissue.
37
How does APO affect the body; respiratory?
- Alterations in capillary pressure, osmotic pressure and alveolar-capillary membrane integrity, results in an increase in fluid in the interstitial space and the alveoli.
- Fluid in the alveoli washes away surfactant, leading to alveolar collapse, reducing surface area for gas exchange which leads to hypoxia.
38
How does APO affect the body; BP?
hypertensive, hypotensive when decompensating.
39
How does APO affect the body; Hepatic?
Hepatomegaly is associated with heart failure. Increased pressure on the hepatic veins prevents adequate drainage of blood from the liver. This causes the liver to malfunction as it becomes congested with blood.
40
How does APO affect the body; Renal?
- Sympathetic stimulation secondary to the heart failure is detected by the kidneys, stimulating RAAS system.
- Results in vasoconstriction and fluid retention which worsens myocardial workload, further worsening heart function.
41
How does APO affect the body; MSK?
- Pitting oedema can be present, this is associated with heart failure.
- The activation of humoral and neuro-humoral mechanisms promotes sodium and water reabsorption and expansion of the extracellular fluid.
42
How does APO affect the body; circulation?
- Due to the reduced cardiac output the sympathetic nervous system is activated resulting in tachycardia. Peripherally shut down, skin is cool and clammy.
43
Define APO
= abnormal accumulation of fluid in the lung tissue, the alveoli space or both.
- results in imparied gas exchnage and decreased lung compliance
- sudden onset of symtpoms
- requires immediate action
44
What are you likely to see on a DRSABCDE assessment of a patient with APO?
A
- frothy sputum indicating partial lower airway obstrution
- cough
- words/short sentences
B
- SOB
- tachopnea
- increased WOB
- hypoxia
- adventitious breathing sounds (crackles)
C
- hypertensive
- tachy
- arrhythmias (cause related)
- pallor , cool and clammy (due to major organ perfusion)
D
- altered concious state
- confusion
- wrestlessness
- ancious
45
WHat is involved in the ongoing management of a pt with APO?
- continuous ABCD
Resp
* manage hypoxia
- Oxygen: maintain saturations >94% (88-92% in COPD)
- Ventilatory support: Non-Invasive Positive Pressure
Ventilation (NIPPV)
Cardiac
* reduce preload and afterload
- Nitrates (GTN): Sublingually or intravenous infusion
- Diuretics (Furosemide): Controversial. IV rather than oral
- Morphine: Lack of good evidence to support efficacy as we know causes resp depression. Manages chest pain and anxiety.
- benzo- in low dose now manages anxiety
Aetiology
* treat underlying cause
46
What is the benefit on nitrates in APO?
- in low doses known to reduce preload
- in larger doses known to reduce afterload
Benifits
- vasodilate vessels thus reducing back up of blood into lungs
- reducing systemic pressure allowing better peripheral perfusion
- decreases blood pressure returning to the lungs
47
What are the benefits of using NIPPV in a patient with APO?
- Ventilatory support for a spontaneously breathing patient
- Improves lung compliance
- Reduces V/Q mismatch (ventilation/perfusion)
- Lowers intubation rates and reduces mortality rate
- Less expensive than intubation
- Fewer complications than invasive mechanical ventilation
48
What are the various types of NIPPV?
1. Continuous Positive Airway Pressure (CPAP)
- one level of pressure on inspiration and exporation
2. Bi Level Positive Airway Pressure (BiPAP)
- Positive End Expiratory Pressure (PEEP)
- the pressure on expiratory pressure is less than inspiratory so feels better.
49
What are some indications fo NIPPV?
* APO (cardiogenic)
* COPD acute exacerbation
* Moderate to severe respiratory distress
* Pneumonia
* Atelectasis
* Dyspnoea
* Accessory muscle use
* SpO2 less than 90%
* Increased respiratory rate (>24 for COPD)
* Respiratory acidosis (pH < 7.35, PaCO2 > than 45 mmHg)
50
What are some contraindications fo NIPPV?
- Uncooperative/ extreme anxiety/ depressed level of consciousness
- Unable to protect airway/ risk of aspiration (impaired swallowing or cough)
- Poor respiratory drive (Head injury)
- Haemodynamic instability
- Myocardial ischaemia/ unstable angina (pressure into intrathoracic cavity impacts this further)
- Copious respiratory secretions
- Difficulty fitting mask (Facial Trauma/ burns/ abnormalities)
- Pneumothorax
51
What are some complications fo NIPPV?
- Hypotension (↑ intrathoracic pressure, ↓ venous return, ↓ CO)
- Myocardial Ischaemia (↑ intrathoracic pressure, ↓ coronary perfusion)
- Altered conscious state (↓ CO, ↓ Cerebral perfusion)
- Risk of aspiration (vomiting)
- Gastric distension (swallowing air)
- Barotrauma
- Pneumothorax (↑ positive pressure and can quickly turn to tension)
- Pressure sores (mask)
52
What are some key points of nursing management of NIPPV?
Response
- Monitor GCS for a decrease
Airway
- Monitor for patency
- Observe for secretions
- Check equipment including suction
- Aspiration risk
Breathing
- Monitor RR / WOB / SaO2 / ABGs
- Assess speech pattern
- Talking in sentences / words / nil
- Auscultate chest
- Nurse in Fowlers position
- Repeated focussed respiratory assessment
- Monitor NIPPV delivery settings
- FiO2, PEEP, IPAP, flow rate
Circulation
- Monitor HR
- Monitor BP
- Cardiac monitor
- ECG
- Monitor urine output
Disability
- 1:1 nurse/ patient ratio
- Monitor GCS
- Assess fitting of face mask
- Pressure area care
- Temperature
- Monitor for nausea
53
Explain the pathophysiology of a pulmonary embolism
= a partial or complete occlusion of a pulmonary artery, or one of its branches, by an embolism.
- The obstruction can be the result of blood clot, air, tumor tissue or fat.
- an emboli that has gained access to the venous system and then pulmonary system where it has stopped and lodged in a narrowing obstructing perfusion of the alveoli.
- due to the high blood flow, the lower lungs are more commonly effected.
- a blood clot forms in the deep veins of the extremities, most commonly in the leg. PE occurs when a portion of the clot from a DVT breaks off, travels through the right heart, and eventually lodges in the pulmonary vasculature
54
What are the complications of a PE?
- pulmonary infarction
- Vasoconstriction of the pulmonary capillaries
- Increased pulmonary artery pressure which may lead to right heart failure
- Increased dead space as perfusion is decreased (V/Q mismatch)
- Decreased surfactant
- Hypoxaemia
- Arrhythmias
- Decreased cardiac output, shock and death
55
What are some risk factors for PE?
- blood clotting from venous stasis
- hypercoagulability
- endothelial injury
- immobility and reduced movement
- surgery within the past 3 months
- history of DTV
- malignancy
- obesity
- oral contraceptives and hormone therapy
- heavy cigarette smoking
- prolonged air travel
- heart failure
- pregnancy
- clotting disorders
56
What are some clinical manifestations of PE?
*depends on size
1. sudden onset pleuritic chest pain
2. SOB
3. Hypoxia
- dyspnoea
- tachypnoea
- tachycardia
- unexplained anxiety
- assess for DVT
- cough
- chest pain
wheezing
- hemoptysis crackles
- synope
- sudden changes in mental status as a result of hypoxia
*note they are related to the sixe and extent of emboli.
57
What are some necessary investigations for PE?
Can be difficult
- history and physical exam
- VTE assessment
- assess clinical presentation
Then
- Venous u/s
- CXR - atelectasis (?collapsed lung)
- ABG- hypoxemia
- ECG (maybe continous)- right heart strain
- CTPA
- CT
- V/Q lung scan
- troponin levels
- pulmonary angiography
58
What are some causes of a PE?
- thrombis emboli
- air emboli (from improperly administered IV therapy),
- bacterial vegetations
- amniotic fluid
- tumours
- fat
- speotic
- heart failure
- overhydration with IV fluids
- Hypoalbuminaemia: nephrotic syndrome, hepatic disease, nutritional disorders
- altered cap permeability of lungs: inhaled toxins, inflammation (e.g. pneumonia), sever hypoxia, near-drowning
- malignancies of the lymph system (e.g. non-hodgkin's lymphoma)
- resp distress syndrome (e.g. )2 toxicity)
- unknown causes: neuro condition, opoid overdose, re-expansion pulmonary oedema, high altitude
- fat emboli (from fractured long bones),
*most commonly embolis origionated in the femoral or iliac veins but also the R) heart particularly in AF and pelvic veins after surgery or child birth.
59
What are some key management points for PE?
- supplementary O2 or intubation
- fibrinolytic agent to disolve source clot
- immediate antocoagulation therapy
- unfractionated heparin IV
- low-molecular-weight heparin
- warfarin for long term therapy
- monitory of aPTT (activated partial thromboplastin time) and INR (international normalised ratio) levels
- limited activity
- surgery to remove clot in those who are fibrinolytic therapy contraindicated
- opioids for pain relief
- inferior vena cava filter
- pulmonary embolectomy in a life-threatening situaiton
- DVT prevention in the first place with compression and anticoagulation meds
- objectives: prevent further growth or multiplication of thrombi, prevent movement, provide cardio support
- may need ventilation support
- resp physio> coughing exercises, turning and deep breating to prevent and support atelectasis (collapsed lung)
60
What are you likely to see on a ABCDE assessment of a patient with PE?
A
- may be obstructions airway if massive so DSABCD/airway support
B
- O2 maintain
- position pt for comfort
- reduce activity and demand on body
C
- Vital signs
- ECG
- IVC
- pathology (ABGs, coagulation, D-dimer, troponin)
- IVT if shock present
D
- GCS,
- PQRST + pain relief to prevent hypoventilation
- prep further investigations
- reassureance
61
What clinical manifestations are you likely to see on assessment of PE: Airway?
- ?patent
- ?obstructed thus unconscious
62
What clinical manifestations are you likely to see on assessment of PE: circulation?
- hypotensive
- tachycardia (compensate for reduce CO)
- reduced cap reil
- pale cool clammy
63
What clinical manifestations are you likely to see on assessment of PE: Breathing?
- Dyspnoea (V/Q mismatch, hypoxaemia)
- Tachypnoea
- ↑ Work of breathing (atelectasis) (due to decreased alveoli tension and thus collapse)
- Hypoxaemia/ Hypocapnia
- Auscultation (clear or some crackles)
- Haemoptysis (blood stained spetum)
64
What clinical manifestations are you likely to see on assessment of PE: Disability?
- anxious/confused
- chest pain (sudden/pleuritic)
- signs of DVT (unilateral leg pain etc.)
65
What is the first line of treatment for PE? and what is the intent of it?
Prevents the formation of new thrombi and allows endogenous fibrinolysis to take effect on the embolus
66
What are possible contraindications for anticoagulation?
- Severe thrombocytopenia (low platelets)
- Active bleeding
- History of haemorrhagic stroke
- Severe hepatic disease
- Bacterial endocarditis
67
What is a commonly used anticoagulant? and what is the administration process?
Unfractionated Heparin (Heparin Sodium):
- IV infusion (+ loading dose based on weight)
- Commenced immediately x 3-5 days
- Dose titrated to APTT as per hospital protocol
68
What are some adverse effects of unfractionated heparin?
- Bleeding
- Bruising
- Hyperkalaemia (aldosterone supression)
- Heparin induced thrombocytopenia
- Allergic reactions
69
What is low molecular weight heparin and when may be it used in the context of PE?
aka enoxaprin
- Subcutaneous
- therapeutic dose (mg/kg) when confirmed PE
- prophylactic dose
- easy for patient to manage
- for Haemodynamically stable PE
- Less frequent monitoring (APTT/ PT usually not increased)
70
What is Vit K antagonist (Warfarin) and when may be it used in the context of PE?
= an anticoagulant
- Oral x 3-6 months
- Long time for therapeutic effect (overlap with Heparin therapy)
- INR monitoring and heparin ceased when in theraputic range
- Recurring PE may require this as lifelong treatment
71
What is Direct oral anticoagulant (DOAC) (Rivaroxaban) and when may be it used in the context of PE?
= direct-acting anticoags
- Quick onset of action (few hours)
- APTT/ PT monitoring not required
- convenient for patients
72
Why and when are thrombolysis' used in the context of PE?
- Accelerates clot lysis (‘clot buster’) to restore pulmonary reperfusion
- Use in massive PE/hemodynamically unstable
- Time critical (4 hours from onset of symtpoms) work best on fresh ones
- High risk of major hemorrhage/ uncontrolled bleeding
- Essential invasive procedures only
73
What are some contraindications of thrombolysis?
- Active bleeding/ bleeding tendency
- Recent stroke (2 months)
- Recent surgery (10 days)
- Recent head trauma (3 months due to risk of intracranial pressure)
- Recent labour/delivery
- Severe uncontrolled hypertension
74
What is an example of a thrombolytic and what are some key points of management?
= Thrombolytic (Alteplase):
- IV infusion (+ anticoagulation follow up)
- Massive PE/ haemodynamically unstable
- Produces local fibrinolysis but has systemic effect which is why it can cause bleeding as a side effect
- Peak plasma time 20-40 minutes
75
Explain when an embolectomy may be used in the context of PE?
- in a Life threatening PE
- Haemodynamically unstable
- Thrombolysis contraindicated
Approach
- Surgical embolectomy (thorocotomy)
- Transvenous catheter to retrieve or break down
- Inferior Vena Cava filter inserted to catch debris
- High mortality rate of 30%
- Risks associated with any surgery
76
What are the treatment options of PE?
- anticoagulation (prevents formantion of new thrombi)
- Thrombolysis/a thrombolytic (breaks clot)
- Embolectomy (removes block)
77
What are some nursing considerations associated with PE?
VTE prevention is a Clinical Care Standard (Australian Commission on Safety and Quality in Healthcare)
Nursing Considerations
- Assessment and documentation of VTE risk
- Identify risk factors
- Venous stasis (reduced mobility, obesity, dehydration, AF)
- Hypercoaguable states (surgery, oestrogen replacement, oral contraceptive pill, cancer)
- Vessel damage (smoking, ↑ cholesterol, varicose veins, venepuncture)
Development of a VTE prevention plan
- Chemical, monitor effects of treatment
- Mechanical (as appropriate e.g. compression socks)
Inform and partner with patients
- Patient education of risk factors, for VTE prevention
78
For the oxygen delivery device: Nasal prongs
What is the min-max flow/min?
Appropriate O2 concentration delivery?
and what are the risks?
Flow: 1-4L
O2 concentration: 22-35%
Risks;
- pressure injury
- Dray nasal mucosa
79
For the oxygen delivery device: Hudston mask
What is the min-max flow/min?
Appropriate O2 concentration delivery?
and what are the risks?
Flow: 5-10L
O2 concentration: 35-60%
Risks;
- pressure injury
- Dray nasal mucosa
- Non-compliance if patient removes device to eat/ talk
- Pressure injury to bridge of nose and ears (strap)
- Aspiration of vomitus
- Claustrophobia
80
For the oxygen delivery device: Non-rebreather face mask
What is the min-max flow/min?
Appropriate O2 concentration delivery?
and what are the risks?
Flow: 10-15L
O2 concentration: >60%
Risks;
- Suffocation if inadequate oxygen in reservoir bag
- pressure injury
- Dray nasal mucosa
- Non-compliance if patient removes device to eat/ talk
- Pressure injury to bridge of nose and ears (strap)
- Aspiration of vomitus
- Claustrophobia
81
For the oxygen delivery device: bag valve mask
What is the min-max flow/min?
Appropriate O2 concentration delivery?
and what are the risks?
Flow: 15L
O2 concentration: varies but 100% in resus
Risks;
?
82
What is the purpose of high flow oxygen delivery?
= deliver oxygen at rates higher than traditional oxygen delivery devices; up to 60 L/minute compared to 15L/ minute
83
What are the pros of high flow?
- more reliable FiO2
- are generally well tolerated by patients
- can be delivered though least invasive form of nasal prongs across the life span
- he high flow rate ensures a continuous flow of oxygen compared to the slower flow devices that allow oxygen to be entrained on inspiration. - This continuous level of oxygen delivery helps to reduce the effort of breathing and may provide some positive pressure in the airways to help with oxygen delivery.
- flow rates that exceed the patient’s peak inspiratory flow demands (so that dilution of delivered oxygen does not occur on inspiration) enabling delivery of a fixed FiO2, irrespective of a patient’s respiratory rate and tidal volume.
- Humidified high flow oxygen delivery is thought to flush out the anatomical dead-space of the pharynx creating a reservoir of fresh oxygen available for the next breath, minimising rebreathing of CO2
- High flow rates may increase the functional residual capacity, reducing work of breathing
- High flow rates may provide a degree of PEEP (4-8 mmH2O)
- Good patient compliance as devices are generally well tolerated by patients
- High flow rates of 10-60L/ minute
- Achievable FiO2 of 21-80%
- Humidification and heating improving mucociliary clearance
84
How does high flow oxygen work?
- an air/oxygen blender connected through a heated humidifier to the nasal cannula, and allows adjustment of the Fio2 independently from the flow rate.
= continuous warm, humidified air.
85
What are some disadvantages of high-flow oxygen?
- risk of complacency if a high FiO2 requirement is not recognised to represent life-threatening illness requiring more than correction of hypoxaemia
86
What are some indications of high flow oxygen?
- Acute hypoxaemic respiratory failure
- Cardiogenic pulmonary oedema
- Prolonged use of oxygen therapy, for example in palliative care
- Patients with either a tracheostomy or laryngectomy
- Mask intolerance in traditional oxygen delivery systems
- Supplemental oxygen delivery for longer than 12-24 hours
