Complete Flashcards
What is the definition of “Assessment”
The action of assessing someone/gathering information
What is the definition of ‘problems’ (actual and potential)?
Signs or warnings of serious complications
What is the definition of ‘interventions’?
Actual treatments and actions/changing the course of action
What is the definition of ‘clinical manifestations/signs & symptoms’?
Results that are either objective or subjective
What is Aetiology?
The underlying cause of a condition or contributing factors
What is pathophysiology?
Altered physiological processes associated with disease or injury - changes in the tissue that result from injury or disease
What is the definition for ‘rationale’?
The explanation/reason for a course of action i.e why something is done
Is the Rapid Assessment Framework considered to be an assessment?
NO
What does the Rapid Assessment Framework Cover
Your ABCDE’s (Airway, Breathing, Circulation, Disability, + environment/exposure) + actual/potential risks
What should the core body temperature of a person be?
Adult: Between 36.5 and 37.7
Older Adult: Between 35 and 36.4
Pedeatrics: Between 37 and 38
What is the expected pulse range for a patient?
10yrs-adult: 55-90bpm
2-10 yrs: 70-110
0-2yrs: 80-150
What is the expected respiratory rate for a patient
Typical: 12-20bpm
3-10yrs: 20-28
0-3yrs: 20-30
What is the expected systolic range for a patient?
<120 mmHg
What is the expected distolic range for a patient?
<80 mmHg
What does 02 stand for?
Oxygen
What does COPD stand for?
Chronic Obstructive Pulmonary Disease
What are red flags?
Signs or warnings of serious complications
What does RR stand for?
Respiratory Rate
What does NZEWS mean?
New Zealand Early Warning Score
What does PaCO2 stand for?
Arterial Carbon Dioxide Tension
What does Sp02 stand for?
Peripheral Oxygen Saturation
What is an intervention?
Actual treatments and actions
What does NP stand for?
Nasal Prongs
What does SOBOE stand for?
Shortness of Breath on exertion
What does V/Q stand for?
Ventilation/Perfusion Ratio
What does TB stand for?
Tuberculosis
What does HC03 stand for?
Bicarbonate
What does PEFR stand for?
Peak Expiratory Flow Rate
What does CPAP stand for?
Continuous Positive Airway Pressure
What does the abbreviation EF stand for?
Ejection Fraction
What does the abbreviation AKI stand for?
Acute Kidney Injury
What does the abbreviation CVA stand for?
Cerebrovascular Accident
What does the abbreviation ARF stand for?
Acute Renal Failure
What does the abbreviation HTN stand for?
Hypertension
What does the abbreviation IHD stand for?
Ischaemic Heart Disease
What does the abbreviation CAD stand for?
Coronary Artery Disease
What does the abbreviation MI stand for?
Myocardial Infarction
What does the abbreviation UAP stand for?
Unstable Angina Pectoris
What does the abbreviation STEMI stand for?
ST-Elevation myocardial infarction
What does the abbreviation AF stand for?
Atrial Fibrillation
What does the abbreviation CHD stand for?
Coronary Heart Disease
What does the abbreviation NSTEMI stand for?
Non-ST-Elevation myocardial infarction
What does the abbreviation HF stand for?
Heart Failure
What does the abbreviation CVD stand for?
Cardiovascular disease
What does the abbreviation PVD stand for?
Peripheral Vascular Disease
What does the abbreviation TIA stand for?
Transient Ischaemic Attack
What does the abbreviation UA stand for?
Unstable Angina
What does the abbreviation CKD stand for?
Chronic kidney disease
What does the abbreviation ACS stand for?
Acute Coronary Syndrome
What does the abbreviation CRF stand for?
Chronic renal failure
What does LOC stand for?
Level of Consciousness
What does ICP stand for?
Intracranial pressure
What does CVA stand for?
Cerebrovascular accident
What does CPP stand for?
Cerebral perfusion pressure
What does TBI stand for?
Traumatic brain injury
What does SCI stand for?
Spinal Cord injury
What does SCBF stand for?
Spinal Cord Blood Flow
What does MAP stand for?
Mean Arterial Pressure
What does SAH stand for?
Subarachoid Haemorrhage
What does BBB stand for?
Blood Brain Barrier
What does CSF stand for?
Cerebrospinal Fluid
What is a pressure injury?
A localised damage to the skin and underlying soft tissue thats usually, but not always, over a body prominence
What type of devices can pressure injurys be caused by?
External medical devices, these wounds are then referred to as medical device-related pressure injurys (MDRPIs)
Can mucous membranes (such as the nose, mouth, lungs, and stomach) sustain pressure injurys?
Yes. Although the anatomy of mucous membrane sites isn’t consistent with pressure injury staging guidelines. For this reason, pressure injuries to mucous membranes can’t be staged using the pressure injury staging system.
What are two examples of where mucous membranes can (such as the nose, mouth, lungs, and stomach) sustain pressure injurys?
- From endotracheal tubes
- From nasogastric tube stabilisers
When does shear occur?
When layers of tissue move in opposite, parallel directions, resulting in stretching, occluding or the tearing of blood vessels and disruption of blood flow to the affected area.
Disrupted blood flow can lead to what?
Tissue ischemia and tissue death
How long can it take to notice a shear injury?
It can take several days for the tissue damage to ‘surface’ and show itself, typically by changes in colour, temperature, and texture
Pressure injurys are staged using what system?
The NPUAP staging system
Do we backstage pressure injurys? I.e saying that an S3PI is healing to an S2PI?
No, once a pressure injury is characterised i.e “S3PI”, it is always that, it can either be a healing S3PI or a non-healing S3PI. If a wound is worsening it can be restaged.
What does HAPIs stand for?
Hospital-acquired pressure injuries
What are the disadvantaged for a patient with a HAPIs?
Higher mortality rate, longer length of stay, and a higher chance of readmission + increased cost of care.
Determining the stage of a pressure injury comes down to what factors?
Presence of fluid in the wound
Colour of the area
Type of tissue exposed or directly palpable.
What are some things we can do as nurses to prevent a HAPI?
Turning and repositioning the patient frequently
Padding bony prominences (pillow between knees ect)
Keeping the elevation of the head at 30 degrees
Ensuring the surface the patient is on allows them to move side to side
Floating the heels off the mattress
Promoting PH-balances skin cleansers followed by moisturisers and protectants
Containing fecal and urinary incontinence to the best we can (pads)
Optimising patients nutritional status
Provide a pressure redistribution mattress and chair pad for those at high risk
Assess for tissue breakdown
Collaborate with the MDT to optimize care interventions.
What is the acronym to use when preventing pressure injuries and what does it stand for?
S - Surfaces and Devices
S - Skin inspection
K- Keep moving
I - Incontinence and moisture
N - Nutrition and hydration
Where on the body are pressure injuries most likely to occur?
Can happen anywhere but Heels, sacrum and ankles are more common
Describe key points to the acronym SSkin inspection to prevent pressure injuries
Carried out regularly (identify any discolouration, change in temperature, swelling and any pain or discomfort)
Pressure mapping can be used to identify the intensity of pressure
Too much bedding can cause pressure and make sure the chair they are using is the chair (sit with knees at a 90 degree angle)
Watch where the feet of tall people are, as the feet might be touching the end and cause pressure
What is the knee break technique?
When moving a client in bed, bring their knees up so there feet are braced on the bed before lifting the head of the bed, so their heels don’t slide along the sheets and cause friction and also help reduce pressure on the sacrum and heels.
Describe key points to the acronym Keep moving to prevent pressure injuries
Having a mobility plan in place helps ensure care is received to meet a person’s needs
The plan should include a repositioning schedule, or walking schedule, aides and people required
Shower and toilet chairs can lead to pressure damage
Describe key points to the acronym Incontinence and moisture to prevent pressure injuries
Incontinence products such as pads, ensure they are changed if full prior to position change as they increase the risk of pressure and skin damage
Someone who experiences incontinence is 40% more likely to sustain a pressure injury
Ensure incontinence products are the right size and shape for the person
Describe key points to the acronym Nutrition and hydration to prevent pressure injuries
Nutrition plays a major part in maintaining optimum skin health. Malnutrition screening and observing what, and the quantity of food and drink taken, and a regular weight check is vital for pressure injury prevention
Overweight people are also at risk. Research suggests in the over 65 age group, as many as 40% are malnourished
How many stages of pressure injuries are there?
4 stages
Stage 1
Stage 2
Stage 3
Stage 4
Characteristics of a stage 1 pressure injury?
Skin is intact with an area of nonblanchable erythema, Meaning when you press on the reddened area, it doesn’t turn white or become pale
Stage one doesn’t describe the layer of tissue that has been impacted, only that localised skin is intact, red and doesn’t blanch
Characteristics of a Stage 2 pressure injury
Partial skin loss with exposed dermis
A wound that is pink or red in colour, consisting of moist, viable tissue
Alternatively, stage 2 pressure injuries can present as an intact or ruptured fluid-filled blister
What stages do nurses confuse with deep tissue pressure injuries?
Stages 1 and 2
How can deep tissue injuries present?
Deep tissue pressure injuries can present as a blood-filled blister or they may have epidermal separation and a darkened wound bed. A deep tissue pressure injury can progress to an unstable wound. When this happens, the wound is recategorised as an unstageable pressure injury
What are deep tissue pressure injuries?
Localised areas that:
Have intact or non-intact skin
Don’t blanch
Are deep red, purple or maroon in colour
What are impairments?
A physical, sensory, neurological, psychiatric, intellectual, or other form that is something an individual has.
What is Disability?
The process which happens when one group of people create barriers by designing a world for only their way of living, taking no account of the impairments other people have
What is a health passport used for?
Its used by people with impairments that may be going from home/care facility to a hospital, its used to communicate the needs of that individual and allows the nurse to provide individualised care to that patient.
What do we need to ensure when working with a patient with an impairment?
Find out about their condition, take the time to find out how to meet their needs, and involve the person with the impairment in planning their care.
What are some examples of types of impairments?
Cerebral palsy, depression, and down syndrome.
what are some things that are important for the safe discharge home of a person with visual impairment?
- Asking the patient about any factors that might affect their ability to preform ADLs or post-hospital recommendations when they are back home. - Then asking this patient about their preferences for accomodating their needs.
- Observe the patient preforming manual tasks independently and without coaching before discharge
- Follow up with the patient shortly after their discharge to determine whether they are successfully preforming self-care activities and to identify any questions or problems.
Define what a long term condition is
- A condition than can be treated and managed, however NOT cured
- A condition that is ‘non-communicable disease’ meaning you can’t catch it
Name some long term conditions
- Autoimmune conditions like diabetes, rheumatoid arthritis
- Chrons disease - not autoimmune however does affect the immune system - inflammatory
bowel condition - Cardiovascular disease
- Cancers
- Respiratory disease
- Mental Illness
- Chronic Pain
- Chronic Kidney disease
- Dementia
- COPD (Chronic Obstructive Pulmonary Disease)
What is the difference between a Long Term Condition and an acute illness?
Therefore Long term conditions are conditions that cannot be cured, however can be managed. An acute illness if treated correctly can be cured. Patients with Long Term conditions can still be admitted to hospital with acute exacerbations of their long term condition. For example Chronic Obstructive Pulmonary Disease (COPD) - acute exacerbation (change in cough or sputum), or heart failure - acute exacerbation
What can empowering patient self-management of their long-term condition do for patients?
- Reduce disease progression - improve their quality of life (QOL)
- Increase the patients understanding of their ‘triggers’ - when they need to get medical help
and from where - Reduce readmission to hospital-reduce costs to health system
Why is it important to understand long term conditions?
- “Chronic illness is the leading cause of morbidity, mortality and inequitable health outcomes in NZ”
- “Reducing the impact of long term conditions is a priority of the NZ health system. Service funders and providers need to be more flexible, innovative and able to measure the difference they are making for their populations. This high-level approach is people/whānau focused, not disease specific.”
What is COPD?
Progressive, chronic disease characterised by irreversible airway obstruction, hindering expiratory flow
Umbrella term encompassing emphysema, chronic bronchitis and other conditions
Each has their own pathophysiology but all contribute to airway inflammation initiated by a noxious irritant
What is Emphysema?
Lung disease which makes it harder for clients to breathe out. The Alveoli are damaged making it harder for effective gas exchange to occur as the air sacs enlarge, Emphysema causes big baggy alveoli (increased volume) so pressure drops – this makes it hard for CO2 to be expelled
What are the 4 major causes/risk factors for COPD cited by WHO
- Tobacco smoking (Cigarettes, pipes, cannabis, second hand smoke)
- Indoor pollutants (Biomass fuel used for cooking and heating (wood and coal) most common in developing countries)
- Outdoor pollutants (Occupational dusts/chemicals, Particulate matter, ozone, sulpha dioxide, nitrogen dioxide, carbon monoxide, and lead (industrialised areas) forest bush fires, agricultural burning, transport
- Genetics, history of respiratory infections
What is Pursed lip Breathing?
It is a ventilatory strategy frequently adopted spontaneously for patients with COPD to relieve dyspnoea (difficultly breathing): it helps to counteract gas trapping. It generates an increased pressure in the airways to allow for expiration (airflow will move from an area of high to low pressure)
How does Pursed Lip Breathing help?
Pursed lip breathing works by moving oxygen into your lungs and carbon dioxide out of your lungs. This technique helps to keep airways open longer so that you can remove the air that is trapped in your lungs by slowing down your breathing rate and relieving shortness of breath
Emphysema causes big baggy alveoli (increased volume) so pressure drops – this makes it hard for CO2 to be expelled. Pursed lip breathing generates increased pressure so that intraluminal pressure exceeds atmospheric pressure and the breath can flow out of the lungs more easily. It is to aid expiration and decrease WOB (work of breathing).
What is Rheumatic Fever and why is it important to discuss?
Rheumatic fever may develop if strep throat or scarlet fever infections are not treated properly or after strep skin infections. Rheumatic fever is thought to be caused by a response of the body’s immune system. The immune system responds to the earlier strep throat or scarlet fever infection and causes a generalised inflammatory response. Strep throat is caused by the bacteria Group A Streptococcus.
If rheumatic fever is not treated promptly, rheumatic heart disease may occur. Rheumatic heart disease weakens the valves between the chambers of the heart. Severe rheumatic heart disease can require heart surgery and result in death.
Is Rheumatic Fever a long term condition?
Rheumatic fever is not a long term condition. Getting a precise diagnosis soon after symptoms show up can prevent the disease from causing permanent damage and can develop into rheumatic heart disease
- Rheumatic Heart Disease is a long term condition
What populations does rheumatic fever impact on more than others?
Although anyone can get Rheumatic fever, It is more common in school aged children (age 5-15), Māori and Pacific children. Rheumatic fever is very rare in children younger than 3 years old and adults. Infectious illnesses, including group A strep, tend to spread wherever large groups of people gather. Crowded conditions can increase the risk of getting strep throat or scarlet fever, and thus rheumatic fever if they are not treated properly. These settings include:
- Schools
- Day-care centres
- Military training facilities
Someone who had rheumatic fever in the past is more likely to get rheumatic fever again if they get strep throat or scarlet fever again
What are the three steps health professions can do for long term condition?
- Primary Prevention
- Reduce disease progression
- Empower patients/whānau
What happens during primary prevention?
Screening - like cardiovascular disease risk assessment, Smear, Well man check, Mammography, vaccinations. Importance of education for primary prevention
What happens during reduce disease progression?
If there are early warning signs of type 2 diabetes, then lifestyle changes can be put into place for example to reverse the high levels of HbA1c back to within normal
What are some important strategies to help support someone with a LTC?
Therapeutic relationship
Acknowledge their challenges, include family
Understand the patients ‘motivators’
Collaborative care approach, education and support.
Look at barriers for the patient
Use a interpersonal approach, use GP, notes, ect
Show compassion and empathy
Empower the patient
Provide patient with as much knowledge about the condition as possible (education)
Support strategies that work for them
What is important steps of discharge planning for a patient with acute exacerbation of LTC?
If patient is admitted with an acute exacerbation of their LTC, the following is important:-
Discharge planning starts as soon as possible following admission
All the correct services are alerted to the admission and kept updated of possible discharge date- INTERPROFESSIONAL COLLABORATION
Community services are restarted on patient discharge.
What does GCS stand for?
Glasgow Coma Scale
What does AEIOU TIPSS stand for? and what is its purpose?
A: Alcohol
E: Epilepsy
I: Insulin
O: Opium
U: Uraemia
T: Tumour
I: Injury
P: Psychiatric
S: Sepsis
S: Stroke
These are some common causes of altered consciousness
What are 7 common causes of falls?
Delirium, cardiac/neurological/muscular-skeletal condition, side-effects from medications, balance/strength/mobility, poor eyesight, poor memory, and incontinence/urinary urgency.
What are the two components that we can divide consciousness into?
Alertness/wakefulness: the appearance of wakefulness
Alertness/cognition: content of cognitive mental functions.
What is the first stimuli assessment we do in the GCS?
Eye opening
Does eye opening mean the patient is aware of their surroundings?
NO
How do we do the first 3 steps of an ‘eye opening’ assessment in the GCS?
Observe the patient before speaking to them. (If their eyes are open, or they open as you approach score a 4 - spontaneous)
Next, talk to the patient with a normal voice, say their name or ask them to open their eyes. (If they open their eyes - score a 3 for speech)
If this fails speak louder or shout. Not touching the pt. (If the patient opens their eyes score a 3 - to speech)
What are the steps after (to speech) that we preform for an “eye opening” assessment?
Next, touch or shake the patient (if the patient opens their eyes score 2 - to pain)
If this fails, use noxious stimuli.
Explain to the patient and family what you are going to do and why, apply a peripheral painful stimulus (applying pressure with barrel of pen to the lateral outer aspect of the second or third interpharangeal joint, gradual pressure 10-15 secs) If the patient opens their eyes score 2 - pain.
If this fails and the patient has still not opened their eyes score 1 - none.
Note: if the patients eyes are closed due to facial injurys or swelling document “C” and a score cannot be assigned for this category.
Verbal responses depend on what in the brain?
Wernickes speech centre which in in the temporal lobe and on broca’s speech centre in the frontal lobe.
What are the steps involved for a “Best verbal response” assessment?
First ask the patient the following questions: ‘Who are you’, ‘Where are you’, and ‘Why are you here’ + ‘What is the current month’ and ‘What is the current season’. - don’t use closed questions. If the patient answers all of these correctly, score 5 - orientated.
If the patient answers one or more of the above questions wrongly but is able to talk in sentences, score 4 - confused. (Orientation to time is often lost first)
If the patient tries to respond to the questions but is unable to talk in full sentences and uses random words or repeats the same phrase or work, score 3
If you hear no intelligible words - score 2. If the patient doesn’t produce any sounds - score 1.
Note: if the patient is unable to respond verbally due to an endotracheal tube, document ‘T’
What are the steps involved for a “Best motor response” assessment? (1-6)
1st. Ask the patient to obey at least two simple commands
Examples: Lift your arms up, hold up your thumb, stick out your tongue. If the patient follows the command, score 6 - obeys commands
If this fails move on. Observe the patient, are they trying to pull their O2 supply ect moving their hand above chin level. This would be ‘localising to pain’ - score a 5.
If both of these are not present we move to applying a painful stimulus. Firstly explain to the patient what you are going to do and why. Apply supra-orbital pressure gradually for 30 seconds, then try the trapezius squeeze for up to 30 seconds.
If the patient try’s to locate the stimulus in an attempt to remove the source of pain, score 5 - localises to pain (note: the patient must bring arm above chin level and across bodys midline). If the patient flexes their arm towards the source of pain but fails to localise or remove it, score 4 - withdrawal from pain/normal flexion. If the patient flexes the arm at the elbow and rotates wrist in response to pain, score 3 - abnormal flexion. If the patient straightens the arm at elbow and rotates it inwards with legs extending and the feet plantar-flexed, score 2 - extension.
If no movement is observed, score 1 - none.
What are some recommendations for clinical practice? GCS
- Listen to the patients family’s concerns
- When communicating a GCS score, state each component of score not just total
- Ensure the same staff member carries out all observations during shift
- at shift handover, observations should be done together with nurse leaving and nurse arriving
- Ask for second opinion when in doubt
- Mark dots not lines on chart
- A drop of one point in motor response is of clinical significance and must be reported to the medical team immediately
- During the night shift, do not assume the patient is asleep and omit assessment
- Clarify with the team the freq of the GCS obs and how long these should be continued for.
How do you do supra-orbital pressure? Are what are the considerations with this type of painful stimulus?
Apply pressure above the eye gradually for a maximum of 30 seconds.
This targets the trigeminal nerve (cranial nerve V), and is contraindicated by orbital damage, skull fracture and glaucoma. This method is also risky for patients with reduced awareness due to potential sudden movement that may cause injury to their eyes.
How do you do the trapezius squeese? Are what are the considerations with this type of painful stimulus?
Apply pressure by grasping approximately 3cm of the muscle between the thumb and forefingers and twisting for up to 30seconds.
This targets the spinal accessory nerve and is documented as the most suitable method. Especially in the presence of orbital damage, skull fracture or glaucoma. Although this method could be difficult on a large or obese patient.
Why are sternal rubs and nail-bed pressures no longer used?
These methods cause prolonged discomfort and damage
Failure to assess the level of consciousness accurately and take appropriate action in a timely manner could lead to what?
Irreversible and devastating consequences
Oxygen (02): monitoring
Sp02, RR, Pa02 (ABG), colour
Oxygen (02): patient education
should include correct administration and use of oxygen delivery devices
Oxygen (02): Adverse effects
toxicity with prolonged exposure to high 02 concentrations; decreased affinity of Hb for C02 in C02 retainers (haldane effect)
Oxygen (02): precautions
oxygen therapy devices should not be used near an open flame due to its high combustibility
Oxygen (02): Pharmacodynamics
oxygen therapy improves effective cellular oxygenation. it acts to restore normal cellular activity at the mitochondrial level and reduce metabolic acidosis
Oxygen (02): pharmacokinetics
oxygen is largely inhaled into the alveoli and diffused into the capillary bed. oxygen combines with haemoglobin, with a small amount being dissolved in the plasma. oxygen is metabolised in the tissues almost entirely in the mitochondria, where oxidase enzymes reduce the oxygen in the formation of adenosine triphosphate (ATP).
excretion of oxygen metabolites (C02 and H20) is via the lung renal system
Oxygen (02): reason
treatment of hypoxaemia by increasing alveolar oxygen tension. The aim is achieve a normal or near normal oxygen saturation for an individual patient
Salbutamol (short acting B2 adrenergic agonist (SABA): reason
bronchodilator - relief of symptoms during maintenance treatment of asthma and COPD; prevention of treatment of exercise/allergen induced bronchospasm
Salbutamol (short acting B2 adrenergic agonist (SABA): monitoring
peak flow measurements before and after administration can help determine effectiveness
Salbutamol (short acting B2 adrenergic agonist (SABA): patient education
what common side effects to expect
appropriate delivery of inhaler (including spacer, mouth care)
asthma and COPD action plan
Salbutamol (short acting B2 adrenergic agonist (SABA): adverse effects
tachycardia, headache, nervous tension, fine hand tremor, hypotension
hyper/hypokalemia (which may cause weakness, fatigue, tremors, muscle spasm)
Salbutamol (short acting B2 adrenergic agonist (SABA): contradictions
caution with CVD, diabetes and HTN
inhaler may contain lactose
Salbutamol (short acting B2 adrenergic agonist (SABA): pharmacodynamics
salbutamol is a B2- adrenergic agonist and stimulates B2 adrenergic receptors. binding to these receptors in the lungs results in relaxation of bronchial smooth muscles
Salbutamol (short acting B2 adrenergic agonist (SABA): pharmacokinetics
onset by inhalation is rapid (5-15 min) peak effect reached in 1-2 hours
metabolised in liver and excreted in kidneys
GTN (Glyceryl Trinitrate Antianginal): Indications for use
Chest Pain/Angina
GTN (Glyceryl Trinitrate Antianginal): Monitoring Requirements
BP and HR
GTN (Glyceryl Trinitrate Antianginal): Patient Education
Sit down, Stand up slowly
GTN (Glyceryl Trinitrate Antianginal): Side Effects
Flushing, Headache, Dizziness, Dry mouth (rare)
GTN (Glyceryl Trinitrate Antianginal): Contra-indications
VIAGRA, ETOH (ethanol), HR <50
GTN (Glyceryl Trinitrate Antianginal): Pharmacodynamics
Antagonises NO receptors = relaxes smooth muscle. Dilates veins and arteries. Reduces BP
GTN (Glyceryl Trinitrate Antianginal): Pharmacokinetics
Sublingual, dermal, rapidly metabolised short duration
Morphine Sulfate: ADDITIONAL NAMES INCLUDE:
Morphine Sulfate (IV), Oxynorm, Sevredol, MS Contin
MORPHINE SULFATE: Indications for use
Analgesia/sedation
MORPHINE SULFATE: Monitoring Requirements
RR, BP, HR
MORPHINE SULFATE: Patient education
Careful mobilising. Avoid ethanol and other opiates
MORPHINE SULFATE: Side Effects
Sedation, Dizziness, Nausea, constipation, hallucinations
MORPHINE SULFATE: Contra-Indications
Respiration rate, depression, severe asthma, acute abdomen pain, traumatic brain injury (TBI)
MORPHINE SULFATE: Pharmacodynamics
Opioid mu-receptor antagonist. Targets CNS opiate receptors. Depresses CNS, RR, GI. Vasodilation
MORPHINE SULFATE: Pharmacokinetics
Oral, IM, IV, Per rectum. Short half life
Define Hypoxia
- Less than normal levels of 02 in the body tissues
Define Hypoxemia
less than normal levels of 02 in the blood
Pa02 <80mmHg (<60mmHg significant hypoxaemia)
Define Hypercapnia
- Greater than normal levels of C02
- PaC02 > 45mmHg
Define Hypocapnia
- Less than normal levels of C02
- PaC02 < 35mmHg
What is the normal range of PaC02?
35-45mmHg
What is the normal range of Pa02 levels?
75-100mmHg
What is the normal range of Arterial Oxygen?
75-100mmHg
What are 12 signs and symptoms of hypoxaemia?
- Changes in the colour of your skin
- Confusion
- Restlessness
- Anxiety
- Increased heart rate
- Increased respiration rate
- Shortness of breath
- Sweating
- Wheezing
- Use of Accessory muscles
- Flaring of nostrils or pursed lips
- Decreased oxygen saturation levels
What are 8 clinical manifestations that a person would experience with COPD?
- Frequent chest infections
- Persistent wheezing
- Persistent chesty cough which can be dry or with sputum
- Difficulty breathing
- Dyspnea
- Decreased energy levels
- Tightness of the chest
- Swelling in the lower extermities
What is efficient gas exchange dependent on?
Adequate Ventilation and Perfusion
What is shunting?
When blood flow can be redirected from poorly ventilate alveolus (one air sac) to a well-ventilated alveolus through vasoconstriction
What is a dead space?
Poor perfusion and a well ventilated alveolus
What is a silent unit?
Poor ventilation AND Poor perfusion (no air moving through the lungs)
What are the two areas of Gas Exchange Insufficiency?
Mechanical
Functional
What are the three areas of Mechanical Insufficiency of gas exchange?
- Structural damage
- Airway obstruction
- Medication
Describe how structural damage impacts on gas exchange
- Nervous system (spinal injury high up, anything that impacts the nerve pathways)
- Intercostal Muscles
- Diaphragm (injury which impacts taking a deep breath to expel CO2 effectively, or on
inspiration with the intake of O2) - Abdominal muscles (Pushing diaphragm out to push the air out)
Describe airway obstruction for gas exchange
- Physiological and foreign objects (asthma, mucous)
Describe how medication can impact on gas exchange
CNS Depressants (Alcohol, benzodiazepines, sedatives. Anything which effects the
respiration rate)
What functional factors can impact on gas exchange?
- Cardiac Compromise (Poor venous return)
- Pulmonary Embolism (Block off blood vessels and lungs - ventilated but not perfused)
- Tumour (blockage which effects perfusion)
- Hb (Haemoglobin) (Not enough Haemogolbin = not enough red blood cells to carry
enough oxygen as Haemogolbin has 4 oxygen particles) - Infection (pus, anything in the lungs which block the perfusion in the lungs)
- COPD
- Compliance (the ability for the lungs to inflate and recoil)
- Resistance
- Surface area (hold the alveolus open, if you lose this, the alveoli might collapse more
easily as the surface area will be reduced - smoking)
What are 4 problems with ventilation (air in/out)?
- Inflammation of Bronchial walls causing epithelial oedema = decrease air entry, decrease gas exchange
- Exudate in lower airways causing obstruction to air flow = decrease air entry, decrease gas exchange
- Exudate in alveoli causing increased diffusion distance = decrease gas exchange
- Inflammation in alveolar wall causing increased diffusion distance = decreased gas exchange
What are 2 problems with perfusion (blood to lungs and body)?
- Partial or complete obstruction to pulmonary artery (could be a clot and partially close off the artery) causing reduced blood flow = decreased gas exchange
- Ineffective functioning alveoli (from exudate or oedema) causing vasoconstriction of surrounding pulmonary capillaries = further decrease gas exchange
What clinical presentations are we observing with the respiratory rate?
- Tachypnoea/bradypnoea (fast and slow breathing)
- Orthopnoea (have trouble breathing lying down, but can breathe normally when sitting up
heart not pumping efficiently) - Dyspnoea (subjective feeling of breathing, reporting they are struggling to breath)
- Rhythm and depth (are they breathing in a normal rhythm? Gasping? Breathing shallow?)
What clinical presentations are we observing with breath sounds?
- Wheeze
- Crackles
- Stridor (usually on inspiration, sounds like a barking type sound. Inflammation or
obstruction of the airway) - Reduced Air entry
- Cough
What accessory muscles are we observing for within the clinical presentation?
- Sternocleidomastoid
- Scalenes
- Trapezius
- Pectoralis minor/major
- Abdominals (on expiration)
What clinical presentation are we observing for the patient’s positioning?
- Upright
- Tripod (leaning forward, supporting upper body with hands on knees/similar)
- Chest symmetry
What are body tissues?
a group of cells that have similar structure and that function together as a unit.
Which usually comes first? Hypoxia or Hypoxaemia?
Hypoxaemia.
We can assess and use interventions to prevent this from going to hypoxia hence preventing cell death
What is a common cause of Hypocapnia?
Hyperventillation.
Taking in too much O2, and not being able to balance this with CO2
What is the cause of Hypoxia?
Often caused secondary to Hypoxaemia.
Which is caused by any condition that reduces the amount of oxygen in your blood or restricts blood flow can cause hypoxia. People living with heart or lung diseases such as COPD, emphysema or asthma, are at an increased risk for hypoxia
What are the medical causes of Hypoxaemia?
ventilation-perfusion (V/Q) mismatch, diffusion impairment, hypoventilation, low environmental oxygen and right-to-left shunting.
What is Ventilation/perfusion mismatch?
Ventilation-perfusion mismatch is mismatched distribution of ventilation (airflow) and perfusion (blood flow)
When does ventilation/perfusion mis match occur?
Ventilation-perfusion (V/Q) mismatch occurs when either the ventilation (airflow) or perfusion (blood flow) in the lungs is impaired, preventing the lungs from optimally delivering oxygen to the blood
What does VQ ratio stand for?
ventilation/perfusion ratio
What is vasoconstriction?
Vasoconstriction is the narrowing (constriction) of blood vessels by small muscles in their walls. When blood vessels constrict, blood flow is slowed or blocked
What is an alveolus?
a small air-containing compartment of the lungs in which the bronchioles terminate and from which respiratory gases are exchanged with the pulmonary capillaries.
What are bronchioles?
A tiny branch of air tubes in the lungs
WOB: 5 signs of respiratory distress
DiapHRaGM
- Diaphoresis (excessive sweating) different to normal sweating, clammy al over dripping in sweat and they feel cold. increased metabolic effort. hypocapnia
- Hypoxia (less than normal level of 02 in the cells
- Respiratory rate
- Gasping associated with running out of breath, RR starts to drop and they start gasping, rhythm changes too)
- Accessory muscle
Need to intervene quickly or they can go into respiratory arrest
what we can measure: RR, depth and pattern
can be measured but a degree of subjectivity depending on how it is calculated
what we can measure: Work of breathing
- accessory muscle use
nasal flaring/ pursed lip breathing - speaking long/short sentences, single words only, not speaking
- intercostal indrawing
what we can measure: peak flow measurement
- measurement of maximal forced exhaled air flow (L/min)
- baseline and to measure effectiveness of interventions
- useful for people with asthma
- used to keep an eye on maximal force
what we can measure: specialist tests
- CXR (chest X-ray)
- spirometry
- CT/MRI
- ABG (arterial blood gas)
Airway assessments
patency is it open and is it fully open, partial obstruction?
- is the airway patent
- partial obstruction- snoring, stridor, you can hear something
- complete obstruction- silence, no extra sounds
- under threat?
- what your assessing for, patency, expecting to find the airway patent, or patent and concern that it is under threat.
possible cause of obstruction
- tongue
- vomit
- epiglottis
- uvulitis
- secretions
- inflammation
- neurological impairment
- foreign body
What is the rationale for “Sitting’ the patient up to increase lung expansion”
In doing this we are increasing ventilation hence increasing gas exchange in the lungs.
What are the 7 things that we can clinically observe when thinking about a patient with a respiratory issue?
Respiratory rate
Breath sounds
Accessory muscles
Positioning
Neurological changes
Skin
Sputum
What are we observing in terms of the Respiratory rate when we are assessing a patient?
Tachypnoea/bradypnoea
Orthopnoea
Dyspnoea
and
Rhythm & Depth
What is Tachypnoea?
abnormally rapid breathing.
What is bradypnoea?
abnormally slow breathing.
What is orthopnoea?
Orthopnea is the sensation of breathlessness that affects a person when they are lying down and subsides in other positions, such as standing or sitting up.
What is Dyspnoea?
difficult or laboured breathing that is self reported by the patient
If we notice cyanosis what is an important factor to assess?
Cyanosis is the blue tinging of the skin so assess capillary refill of peripherals.
What is a peak flow measurement test?
Peak flow is a simple measurement of how quickly you can blow air out of your lungs. Normal adult peak flow scores range between around 400 and 700 litres per minute
What can we use a peak flow measurement for?
as a baseline and to measure the effectiveness of interventions (useful for diagnosing asthma)
What are clinical presentations of neurological changes?
Anxiety
Agitation
Confusion
Drowsiness
Pain
What are clinical presentations of Skin?
Diaphoresis
Pallor
Cyanosis
Flushing
What are clinical presentations of Sputum?
Colour
Odour
Haemoptysis
Airway interventions:
Positioning:
- maintaining head and neck alignment (chin tilt/jaw thrust)
- Consider elevating head of bed/side positioning in OSA
- Recovery position
Clear secretions:
- Encourage airway clearance with coughing
- Consider suctioning (Yankeur/suction catheter)
- Promote hydration to thin secretions for expectoration
Breathing assessments:
General appearance:
Work of breathing
Rate, depth and pattern
Accessory muscle use
Nasal flaring/pursed lips
Cough
Colour
Skin moisture
Positioning:
Supine/erect
Tripod
Pillows to support
Level of activity:
What is your patient doing?
Chest:
AP measurement
Symmetry
Paradox
Drains?
Supplemental oxygen use:
Nasal cannula
Airvo (humidified O2)
CPAP/BiPAP machine
Posterior chest auscultation:
Air entry
Quality of breath sounds
Wheeze
Crackles
Adventitious sounds
Percussion:
Resonance
Hyper resonance
Dullness
Breathing interventions:
Positioning:
Sit the patient upright
Support with pillows if required
Mobilise as able
Regular turns/repositioning
Cough techniques:
Huff coughing
Incentive spirometry
Deep breathing
Administer prescribed medications:
Bronchodilators (inhalers with spacer
Oxygen
Physiotherapy referral:
Education
Loosen secretions
Secretions:
Promote hydration to thin secretions
Consider humidification of O2
Anxiety reduction:
Education and reassurance to reduce respiratory effort and SNS response
Circulation assessments:
General appearance:
Skin colour
-Flushed
-Cyanotic
Temperature
-Raised (core)
-Peripherally cool
Capillary refill time
Diaphoresis
Heart rate:
Tachycardia/bradycardia
Rhythm (regular/irregular)
Quality (weak/bounding)
Blood pressure:
Hypertension
Normotension
Hypotension
Renal function:
Urine output
eGFR
Fluid balance
Circulation interventions:
Hydration:
Oral
Intravenous fluid as prescribed
Administer prescribed medication:
Consider DVT prophylaxis
Mobilising:
Foot pedalling
Frequent mobilisation as able
Regular repositioning
Disability assessments:
Level of consciousness:
AVPU
Orientated to time, person & place?
Restlessness/agitation (hypoxaemia)
Anxiety:
Breathlessness
Fear of dying
Dyspnoea
Increased work of breathing
Mood
SNS response
Pain:
COLDSPA
Pleuritic pain will contribute to alveolar hypoventilation (decreasing gas exchange)
Opioid analgesia causing ↓ RR and LOC
Disability interventions:
Pain management:
Select appropriate analgesia
Administer analgesia as prescribed
Anxiety reduction to reduce SNS response:
Patient education
Communication of plan
Involve family/whānau
Not “reassure patient” – what does this mean?!
Environment assessment:
Patient risk assessment:
Falls
Braden
Smoking
Past medical/surgical history:
Previous respiratory issues (COLDSPA)
Medications
Drug reactions
Allergies
Early Warning Score:
Trends
Action required?
Other assessments:
Occupation (hazards)
Living situation
Family/whānau supports
Self-management of health issues
Alcohol and drug use
Cultural needs
Spiritual needs
Define Heart Failure
An acute or chronic condition in which the heart doesn’t pump blood as well as it should resulting in congestion (CHF) of blood backing up and unable to meet the demands of the body
- The heart’s inability to consistently pump enough blood to organs and tissues
- Cardiac output is insufficient to meet the metabolic demands of the body and accommodate venous return
- Occurs from either a structural or functional abnormality of the heart
- The resulting decreased blood supply to body impairs organs and tissue function
- The dominant feature is inadequate tissue perfusion
What is a structural abnormality of the heart?
Valve problem/dysfunction, ventricle thickness, rigidity
What is a Functional abnormality of the heart?
Following a MI, cardiomyopathy, CAD (coronary artery disease)
Define Cardiac Output (CO)
Stroke Volume x Heart Rate (3.5-5L/min)
Define Stroke Volume (SV)
Amount of blood pumped out per heartbeat
Define Preload
(Volume) amount of ventricular stretch at the end of diastole. The greater the stretch the stronger the contraction (Starling’s Law)
Define Afterload
(Pressure) resistance to the ejection of blood from the ventricle
Define Ejection Fraction, what the normal is and how it is measured
- The ejection fraction (EF) is the amount of blood that is pumped out of the left ventricle (LV) with each heartbeat
- A decreased EF = decreased amount of blood being pumped out = decreased perfusion
- It is measured in percentages
- Normal range is 55-70%
- An EF of 40% or less indicates HF
- Calculated from an echocardiogram
What is Systolic Heart Failure?
- Shortened to HFrEF which stands for Heart Failure reduced Ejection Fraction
- Pumping problem of the heart
- Inability of the Left ventricle to contract effectively
( Ventricles can’t pump hard enough during systole )
What is diastolic heart failure?
- Shortened to HFpEF which stands for Heart failure Preserved ejection fraction
- It is a relaxing problem
- Inability of the Left ventricle to relax and fill effectively
( Not enough blood fills into ventricles during diastole )
Define systole and diastolic
Systole = The ventricles eject blood (pump)
Diastolic = The ventricles fill with blood (relax)
What is Right-Sided Heart Failure?
- The right ventricle cannot eject sufficient amounts of blood - blood backs up in the venous system and may result in:
- Peripheral Oedema
- Weight gain but anorexia/nausea may be present
- Hepatomegaly/Splenomegaly
- Liver is the last place to send blood back to the heart
- Ascites
- Jugular vein distention
- The blood can back up to the rest of the body via the right atrium and manifest as oedema, legs/ankles/feet, sacrum/penis (dependent areas) around the eyes, organ oedema
(Could experience Anorexia, GI distress, Weight loss, signs related to liver function impairments)
What is Left-Sided Heart Failure?
- The left ventricle cannot pump blood effectively to the systemic circulation. The blood backs up in the pulmonary system so the pulmonary venous pressure increases in:
- Decrease EF
- Pulmonary congestion/oedema with dyspnoea
- Cough
- Crackles
- Impaired oxygen exchange
- LHF is the most common form (from left ventricular dysfunction). Blood cannot get out and around the body, so it backs up in the lungs via the left atrium and pulmonary vein
- It causes pulmonary congestion and oedema in the lungs
(cough with frothy sputum, Cyanosis and signs of hypoxia, orthopnea)
What is the patho for Heart Failure?
- MI or cardiac dysfunction/structural abnormality impairs ability of L) ventricle to fill with or eject blood
- Poor ventricular function/myocardial damage leads to decreased stroke volume and cardiac output
- Leads to a neurohormonal response
- Either sympathetic system is activated to increase cardiac workload, or RAAS pathway is activated
- Results in vasoconstriction and sodium + fluid retention
- Further stress on the ventricular wall and remodelling leads to heart failure
What are some signs and symptoms of heart failure?
Pale, grey, SOBOE, orthopnea (unable to lie flat and breathe), nocturia (increased urination overnight due to lying flat and kidneys being well perfused), oedema, confusion, tachycardia, hypotensive, dry cough, dyspnoea, weak pulse, tachypnoea, fatigue, anxiety, ECG abnormalities, palpitations, restlessness, hypoxaemia, moist cough, diaphoresis, cyanosis, dizzy, light-headed, nausea, weight-gain, SOB, crackles on auscultation, ascites, exercise intolerance
What are some risk factors/aetiology for Heart Failure?
- Ischaemia - Myocardial infarction (elevated Troponin)
- Valve disease
- Cardiomyopathy
- Pericarditis
- Fluid overload (renal failure, Intravenous fluid (IVF))
- Hypertension
- Smoking
- Type 2 Diabetes
What is an echocardiogram?
a test of the action of the heart using ultrasound waves to produce a visual display, for the diagnosis or monitoring of heart disease.
What is an LVEF?
Left ventricular ejection fraction (LVEF)
Ejection fraction typically refers to the left side of the heart. It shows how much oxygen-rich blood is pumped out of the left ventricle to most of the body’s organs with each contraction.
Which usually occurs first? LHF or RHF?
LHF usually develops first then RHF because the left ventricle pumps blood throughout the body.
What does TNI stand for?
Troponin I
These are proteins that are released when the heart muscle has been damaged, such as occurs with a heart attack
What is valve disease?
In heart valve disease, one or more of the valves in your heart doesn’t work properly.
What is cardiomyopathy?
Cardiomyopathy is a disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body.
What is pericarditis?
Pericarditis is swelling and irritation of the thin, saclike tissue surrounding the heart (pericardium). Pericarditis often causes sharp chest pain.
what are the clinical manifestations (symptoms) of left sided HF?
Dyspnoea (difficult or laboured breathing)
Orthopnoea (Discomfort when breathing while lying down flat)
Paroxysmal nocturnal dysponea (a sensation of shortness of breath that awakens the patient)
Pulmonary congestion - cough, crackle, wheeze
What are Compensatory Mechanisms?
Baroreceptors in the aortic and carotid arteries sense a drop in the BP
The sympathetic nervous system (SNS) releases adrenaline and noradrenaline
Low cardiac output and vasoconstriction results in decreased renal perfusion → renin is released by the kidneys
This initiates the renin angiotensin aldosterone system (RAAS)
What do the compensatory mechanisms result in?
SNS activation results in:
↑ Heart rate and ↑ contractility which ↑ blood pressure
Neuro-hormonal activation results in:
↑ blood volume (related to aldosterone & ADH secretion) which ↑ preload angiotensin II ↓ vascular capacity which ↑afterload
What are the consequences of Heart failure?
Pathophysiological process:
↓ blood & O2 supply to
body (pump failing)
SNS & RAAS response
helps… but ultimately
harms
Signs and symptoms:
Shortness of breath
Orthopnoea/nocturia
Oedema - peripheral/pulmonary
Exercise intolerance
Fatigue
Weight ↑
Attempts to ↑cardiac output to ↑O2 delivery:
tachypnoea
tachycardia (risk of arrhythmias
What sided Heart failure would it be if the patient has puffy ankles?
Right as RV is failing to pump the blood forward to the lungs, backing up in the body via the RA
What sided heart failure would it be if the patient has crackles/fluid in the lungs?
Left as LV is failing to pump the blood forward to the body, is backing up in the lungs via the LA
What are the goals of management?
Treat the underlying cause if possible
Aim to increase cardiac function and decrease myocardial workload – beta blockers
Prevent harmful neuroendocrine responses, e.g.. SNS, RAAS, ventricular remodelling – ACE inhibitors.
What is the difference between Acute and Chronic HF?
ACUTE i.e. post surgery fluid overload – common in the elderly – correct the cause with diuretics and it goes away
CHRONIC i.e. r/t myocardial dysfunction caused by IHD, cardiomyopathy, HTN or valvular disease/disorders
Why would a patient with MI may get HF?
Damage to the myocardium esp LV – is a piece of steak – ineffective pumping. Depending on the extent of the infarction that would affect the severity of the HF
Chronic Heart Failure
Heart failure is commonly caused by IHD
It is common in the elderly – one of the main reasons for admission to hospital
The pathological processes that underpin heart failure result in decreased contraction, decreased filling or both.
How would you know if someone has HF?
Statements of:
c/p, heavy weight, indigestion, SOB, SOBOE,
Increased HR (to pump more oxygen around body)
BP low
Ability to speak
ECG
Oxygen saturations and/or ABG
Cyanosis/colour/diaphoresis
Sounds (gurgling/snoring/apnoea)
Agitation/confusion
Anxiety
Dyspnoea
What assessments would you use for someone with HF?
Rapid Ax, Posterior Chest Ax, Peripheral vascular Ax, Apical pulse – PMI, if sond displaced then eg of ventricular hypertrophy.
Juglar Venous Pressure (JVP) measurement
The vein acts as a barometer to measure fluid in the right atrium
Raised JVP indicates fluid overload
Common in right sided heart failure.
What are the functions of the kidney?
- Remove waste products from the body by turning them into urine
- Remove drugs from the body
- Balance the body’s fluids
- Release hormones that regulate blood pressure (renin, erythropoietin)
- Produce an active form of vitamin D that promotes strong, healthy bones
- Control the production of red blood cells
- Electrolyte Regulation
WWETBED.
What is Glomerular Filtration Rate?
Glomerular filtration rate (GFR) is the amount of blood that passes through the glomeruli each minute
The normal blood flow through the kidneys is 105-125 mls/min →99% is reabsorbed resulting in 1- 1.5L of urine per 24 hours
What are the 3 factors needed for urine production?
Pre-renal:
Adequate perfusion pressure (renal blood flow) and oxygenation of kidneys. If there isn’t enough pressure in the system then urine output will decrease. The kidneys may be functioning fine but if the system isn’t functioning well
Renal:
The kidney units must be functioning properly i.e. no damage to the structures in the kidney such as tubules, glomerular
Post-renal:
There must be no obstruction to urine flow
What is Oliguria?
Low Urine output. 100-400ml/day (an early warning sign related to poor urine output)
What is Anuria?
Lack of urine production. A late warning sign related to poor urine output. <100ml/day
How many hours of Oliguria can cause acute kidney injury?
Two hours
What is an acute kidney injury?
Acute kidney injury (AKI)occurs when the kidneys are unable to remove the body’s metabolic waste or perform their seven regulatory functions, in particular, Maintenance of BP and electrolyte regulation. These metabolic wastes build up in the body and GFR falls as the disease progresses
What are the three causes of Acute Kidney Injury?
Pre-Renal Causes: (Low cardiac output, low BP, severe vomiting)
Intrarenal (Intrinsic) causes (Damage to renal tissue, nephrotoxins, NSAIDS (Non-steroidal anti-inflammatory drugs)
Post-renal causes (Obstruction (kidney stones), renal calculi)
What are the 4 phases of Acute Kidney Injury and how long do they occur for?
Initiating phase hours = days
Oliguric phase = 10 - 14 days
Diuretic phase
Recovery phase = 3 - 12 months
What nursing assessments would you undertake for Acute Kidney Injury?
- Fluid balance chart (FBC)
- Daily weigh (1kg of weight = 1L retained fluid)
- Skin integrity
- Vital signs → EWS
- Capillary refill time (CRT)
- Palpate and/or scan the bladder
- Bloods – GFR, electrolytes, CBC
- Ability to manage ADLs
What are the 2 types of dialysis?
Haemodialysis
Peritoneal dialysis
What is Haemodialysis?
A machine removes blood from your body, filters it through a dialyser (artificial kidney) and returns the cleaned blood to your body. This 3- to 5-hour process may take place in a hospital or a dialysis centre three times a week.
What is Peritoneal dialysis?
During peritoneal dialysis, a cleansing fluid flows through a catheter into part of your abdomen. The lining of your abdomen (peritoneum) acts as a filter and removes waste products from your blood. After a set period of time, the fluid with the filtered waste products flows out of your abdomen and is discarded.
What needs to happen for BP to remain stable?
Need a fully functioning myocardium and kidneys
What are some risk factors for chronic kidney injury?
Diabetes
Hypertension
Smoking
Obesity
Ethnicity
Gender men>women
Age - kidney function decreases with age
Specific conditions – glomerulonephritis
What is Chronic Uramia?
Built up waste in the kidneys which the body wants to get rid of
What are the Nursing Interventions for renal?
Maintain adequate nutrition
Fluid restriction
Promote activity & rest as tolerated
Provide skin care
Provide education on condition & complications
Provide culturally appropriate care
Psychological/emotional l support
Support for smoking cessation
What are the treatment aims for renal?
Treatment is aimed at slowing the progression of the disease
Smoking cessation
Adequate BGL control
at least two alcohol free days per week
Reduce systolic BP by
reducing the BMI
moderate physical activity
reducing salt intake
What are the gerontological considerations in acute kidney injury?
Care with medications due to ↓renal function (e.g. ↓GFR & ↓nephrons)
Reduced organ function due to the normal ageing proccess
Co-existing conditions (e.g. diabetes, HF)
Polypharmacy
Dehydration (& hypotension) are poorly tolerated (care with diuretics) as is fluid overload
Older people are less able to maintain homeostasis due to cellular ageing
What is the difference between CKI and AKI?
AKI tends to cause sudden, severe symptoms that are easily recognised, while CKD symptoms develop slowly and are easily mistaken for other conditions. While AKI can usually be reversed by resolving the underlying cause, CKD is not reversible and need to be managed to preserve the function of the kidneys. AKI is often associated with medications such as morphine and ibuprofen
What are some causes of Neurological Deterioration?
- Alcohol
- Epilepsy
- Insulin
- Opiates
- Uraemia
- Tumour
- Injury
- Psychiatric
- Stroke
- Sepsis
(AEIOU TIPSS)
What is Increased intra-cranial pressure (ICP)?
Occurs when there is an imbalance inside the cranium, following brain injury or other medical conditions that cause an increase in pressure inside the skull.
What are the main elements generating ICP?
Brain tissue, blood volume and cerebrospinal fluid (CSF)
What is the patho of raised ICP?
A rise in ICP greater than cerebral perfusion pressure, (CPP), results in reduced blood flow to the brain as vessels are squashed from the pressure
Reduced blood flow = reduced oxygen and glucose delivery which results cerebral ischaemia.
What is the Monro-Kellie Hypothesis?
States that the sum of volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood is constant
An increase in one should cause a reciprocal decrease in either one or both remaining two
What is Cushings Triad?
- Rise in ICP greater than CPP causes reduced blood flow to the brain. Reduced blood flow means less O2/glucose delivery to tissue causing cerebral ischaemia.
- Cerebral ischaemia stimulates a sympathetic response (adrenaline release to increase BP & HR) in order to increase blood flow and therefore O2 delivery
- Parasympathetic response initiated by increase BP is detected by baroreceptors. This results in an attempt to reduce BP by decreeasing HR
- Ongoing increased BP causes further rise in ICP and further restriction of blood flow. A switch of aerobic cellular respiration to anaerobic respiration results in decreased ATP production for cellular function (cerebral ischaemia)
- Breakdown of Na+/K+ pump causes water to enter the cell, resulting in cell death. As cerebral oedema worsens, the brainstem is compressed causing irregular respirations before death is imminent
What are the early signs of raised ICP?
Confusion
Drowsiness
Headache
Forgetfulness
Limb weakness
Nausea
Photophobia
Diplopia
Oval pupils (from round)
Impaired extra-ocular movement
What are the late signs of raised ICP?
Projectile vomiting
Seizures
Fixed and dilated pupil/s
Loss of gag reflex
Abnormal flexion/extension of upper and lower limbs
Hypertension (widening pulse pressure)
Bradycardia
Irregular respiratory pattern
How would someone’s LOC be with raised ICP?
Drowsiness
Lethargy
Dizziness
How would someone’s speech be with raised ICP?
Slurred (dysarthria)
Delayed
Word finding difficulty (expressive/receptive dysphasia)
No speech (aphasia)
How would someone’s motor strength be with raised ICP?
Mild/mod/severe weakness
Hemiplegia (one sided arm/leg/face weakness)
Sensation changes
Swallowing difficulties (dysphagia)
Uncoordinated
How would someone’s behaviour be with raised ICP?
Disinhibition
Personality change
Emotional
How would someone’s pupils be with raised ICP?
Unequal
Sluggish
Oval
Pinpoint
How would someone’s cognition be with raised ICP?
Poor memory
Inability to sequence
Change in comprehension
Confusion
What are the two priority assessments you would preform to assess neurological function?
AVPU
GCS
What does the brain need to function?
Oxygen and glucose
- when body is resting brain uses 20-25% of oxygen & glucose
Blood flow
- interruption causes irreversible damage within 3-8 minutes
Electrical conduction
- relay and process information
What is autoregulation?
A way of maintaining brain blood flow despite changes in cerebral perfusion pressure (the pressure required to deliver adequate oxygen and glucose)
Once cerebral perfusion pressure (CPP) is outside the range of 60-160mmHg, autoregulation is lost
If autoregulation is lost, the brain relies on mean arterial pressure (MAP) to maintain it’s blood supply
This means that if there is injury to the brain and a patient’s blood pressure is too low, there is not enough pressure to drive the blood around the brain
↓ oxygen ↓ glucose = brain tissue hypoxia and death
What are other neurological assessments?
Nervous system assessment
-Cranial nerves (CNI – XII)
-Spinal nerves (C1-8, T1-12, L1-5, S1-5, Co1)
–Reflexes
–Sensation
–Strength
Coordination and balance
Gait
Mini mental state examination (MMSE)
Speech and language
What are some diagnostic tests include?
Computerised tomography (CT)
Magnetic resonance imaging (MRI)
Carotid ultrasound/Doppler (measures cerebral blood flow)
EEG – electroencephalograms (electrical activity in brain)
Cerebral angiography: identify responsible blood vessel
Lumbar puncture for CSF analysis (can also be sampled
from ventricles)
Pharmacotherapy - cva
Antiemetics
May provide nausea relief
Antipyretics
Reduce metabolic activity
Diuretics
Control fluid balance
Corticosteroids
Reduce cerebral oedema
Antiepileptics
Control of neurotransmitters
Thrombolytics
Fast dissolution of blood clots
Antiplatelets
Prevents platelets from sticking together and clumping
Analgesics
Reduce SNS activity and reduce ICP
Skeletal muscle relaxants
Ease contractures
Anti-parkinson
Increase dopamine/reduce acetylcholine activity to improve motor coordination
Faecal Softeners
Prevent straining and increasing ICP
Antibiotics
Reduce systemic inflammation and cerebral oedema
Antiarrhythmics
Improve cardiac output and cerebral perfusion
Antihypertensives
Prevent secondary cerebral ischaemia through raised ICP
Define stroke
Rapidly developing clinical signs of focal (or global in case of coma) disturbance of cerebral function
Lasting more than 24 hours or leading to death
What is the aetiology of a stroke?
Hypertension, Age, Drugs/alcohol, Females have an increased risk due to Oestrogen, Inactivity, Obesity, Diabetes, High cholesterol
What are some symptoms of a stroke?
Trouble walking, trouble speaking and/or understanding, one-sided weakness or paralysis
Motor deficits (mobility, swallowing, gag reflex, respiratory)
Communication (speaking, aphasia)
Intellectual function (memory, judgement)
Affect (trouble controlling emotions
What are some nursing interventions for a stroke?
Maintain head of bed 30 degrees:
to facilitate jugular venous drainage and help reduce intracranial pressure
Maintain systolic blood pressure within prescribed parameters (often < 180mmHg):
to reduce the potential for further bleeding or ischaemic changes
Continuous neurological observations:
to help identify deterioration to initiate timely intervention and treatment
Ensure correct positioning of paralysed limbs:
to prevent contractures and maximise function for rehabilitation
Ensure patient is kept NBM until swallow is assessed by Speech and Language Therapist:
to prevent aspiration of oral fluid and food
Administer prescribed aspirin orally or enterally:
to impede clotting and prevent further ischaemia
Turn the patient regularly:
to maintain skin integrity and prevent pressure injury if the patient cannot move themselves
What are the two main types of stroke?
Ischaemic and Haemorrhagic
What is a cerebral embolism? (Ischaemic stroke)
Cerebral embolism is a blood clot or debris formed elsewhere in the body which travels to the brain. If it cannot pass through the lumen it will occlude the vessel, interrupting blood flow causing tissue ischaemia.
What is a cerebral thrombosis? (Ischaemic stroke)
Cerebral thrombosis is a narrowing of the cerebral arteries caused by plaque build-up. A clot then forms on the plaque, occluding the vessel lumen and restricting blood flow to an area of the brain. Tissue ischaemia results if not thrombolysed.
What is a Haemorrhagic stroke?
A burst blood vessel will cause blood to leak into brain tissue and surrounding structures, causing a rise in intracranial pressure and damage to brain tissue
What is the patho of a Ischaemic Stroke?
Ischaemic Cascade
Disrupted blood flow
Anaerobic respiration
Lactic Acid
Insufficient ATP
Ion imbalance
Increase in intracellular calcium
Increased Glutamate
Vasoconstriction
Enlarged area of infarction into penumbra*
Cell membrane and proteins break down
Formation of free radicals
Protein production decreased
Cell injury and death
What is the patho of an Haemorrhagic stroke?
Ruptured vessel
Explosive eruption of blood from vessel into surrounding brain tissue and structure
Haematoma develops
Exposure of brain to blood, an increase in intracranial pressure caused by sudden entry of blood into the tissue, and secondary ischaemia result from reduced blood flow/perfusion
Ion imbalance
Mismatch between blood flow and metabolic demand
Breakdown of sodium/potassium pump maintaining cellular function
Anaerobic respiration to produce ATP
Increased production of lactic acid
Cell death
Altered pH
Cell membrane and proteins break down
Formation of free radicals
Cell injury and death
What can brainstem strokes lead to?
Coma
Breathing problems, spontaneous changes in blood pressure and heart rate
Nausea and vomiting
What symptoms can cerebellar strokes cause?
Ataxia, dysarthria, incoordination, nystagmus
What happens in a R) sided brain injury?
Paralysed left side
Special perceptual deficits
Quick, impulsive behavioural style
Memory deficits
Short attention span, impulsive (safety concerns), impaired judgement (tends to minimise problems), impaired time concepts
What happens in a L) sided brain injury?
Paralysed right side
Speech and language deficits
Slow, cautious behavioural style
Memory deficits
Aware of deficits (more prone to anxiety, depression), impaired comprehension r/t language/mathematics
What is a Transient ischaemic attack (TIA)
A temporary focal loss of neurological function caused by ischaemia (less than 24hrs)
Most resolve within 1-2 hours
Result from inadequate blood flow to brain from partial or complete occlusion of an artery
What is a spinal cord injury?
Mechanical disruption to the structure & function of the spinal cord & spinal nerve pathways.
Can be a traumatic or non traumatic injury
What causes a traumatic spinal cord injury?
Damage to the spinal cord resulting from a traumatic event, fall or accident usually occurs from a fracture and/or dislocation of the spine. May also be the result of penetrating injuries from:
displaced bony fragments penetrating the spinal cord and/or the spinal nerves. bullets or weapons.
What causes a non-traumatic spinal cord injury?
Vascular disorders, tumours, infections or haematomas causing cord compression
What are the types of spinal cord injury?
Transient concussion (reversible)
Contusion (bruising)
Laceration (cut to the cord)
Compression (Squashed)
Transection (irreversible, cut through the cord)
What are some of the symptoms of a spinal cord injury?
Symptomsdepend ondegree of paralysis & potential for rehabilitation depends on the level of lesion
Paralysis from below level of injury
Loss of reflexes
Loss of bowel, bladder and sexual function
Muscle spasm
Inability to control body temperature
Loss of bone density
High risk of pressure injury
What is the patho of a spinal cord injury?
Microscopic haemorrhages occurs in the central grey matter and pia matter
Tissue volume is increased, causing compression and necrosis
Oedema occurs in the white matter, causing impaired circulation throughout spinal cord
The haemorrhage and oedema obstruct blood flow and lead to further ischaemic areas
Leads to functional impairment which may be temporary or long term
What are some nursing interventions for spinal cord injuries?
Encourage independence but assist with ADLS
Assist with bowel/bladder cares
Prompt pressure area cares
Regular position changes
Ensure environment is clutter free
Provide education surrounding rehab
What are some secondary spinal cord injuries?
Ischaemia
Hypoxia
Oedema
Inflammatory Process
What functions will be lost with a complete spinal cord injury?
Voluntary movement
Sensation of pain, temperature, pressure & proprioception
Bowel and bladder function
Loss of reflexes
What vertebrates are important in testing motor function?
C5-Elbow flexion L2-hip flexion
C6-wrist extension L3-knee extension
C7-elbow extension L4-ankle dorsiflexion
C8-finger flexion L5-toe extension
T1-finger abduction S1-ankle plantar flexion
What are the complications of spinal cord injury?
Spinal Shock
Neurogenic Shock
Autonomic Dysreflexia
What is Spinal Shock?
Areflexia (sudden depression reflex activity) < level injury
Muscles paralysed, flaccid and without sensation below level of injury
Bowel and bladder function lost
Gastric stasis
Paralytic ileus
What is Neurogenic Shock?
Loss of autonomic control leads to:
- ↓ BP, ↓ HR
- Peripheral venous pooling
- Priapism
- Loss of temperature control
- Lack of perspiration below level of injury
What is Autonomic Dysreflexia?
Occurs after spinal shock has resolved in persons with SCI above T6. Stimulus causes sympathetic nerves to become overactive
inhibitory nerves from brain travelling down spinal cord serve to moderate all spinal cord reflexes thus if someone taps your knee - your leg kicks. This is a spinal reflex
Simple response to painful stimulus makes your body react with reflexive sympathetic response at spinal cord level as well as increasing B/P. Normal circumstances inhibitory nerves from brain moderate response.
What is the possible aetiology of Autonomic Dysreflexia?
Urinary retention
Over distended bladder or bowel
Pressure ulcers
Kidney stones
Ingrown toenail
What is the patho of Autonomic Dysreflexia?
Noxious stimulus (distended bladder, constipation etc.)
Signals transmitted to spinal cord to initiate SN activation (> HR, > BP - vasoconstriction, > RR)
HTN stimulates baroreceptors in carotid bodies. Brain initiates PN activity to reduce BP by slowing HR (bradycardia)
Signals to reverse SN activity sent from brain via spinal cord to vasodilate blood vessels, slow HR. This occurs ABOVE SCI level
Signals can’t pass BELOW level of injury.
If noxious stimulus continues, ascending signals continue to initiate SN activity
Results in increasing HTN (associated headache, blurred vision) bradycardia, vasodilation ABOVE SCI level and vasoconstriction BELOW
What are the signs and symptoms of autonomic dysreflexia?
HTN (>20mmHg Pt baseline) bradycardia
Headaches
Blurred vision
Facial flushing
Diaphoresis above level of injury
Anxiety and restlessness
What are the nursing interventions for Autonomic Dysreflexia?
Put the person into sitting position 90◦ to help lower the BP
Loosen clothing
Assess for the probable cause and remove
Continue to assess vital signs (Q2-3min BP)
Administer GTN as prescribed if SBP > 150mmHg (short acting anti-hypertensive medications only)
Preoperative considerations
- Vital signs
- Preop checklist guiding document for before patient goes to surgery
- NBM status nil by mouth status (have to have fasted 6 hours before surgery)
- Medications (what they can and cant have, blood thinners is a no)
- Consent
- Weight and height (if necessary, necessary for anastatic/medications) (important for appropriate dosing of medication, especially for anastatic)
- Specific physical assessments (how well they are physically will determine how well they will do during surgery)
- Neurovascular
- Neurological (GCS/ PERRLA/ limb strength)
- Respiratory / cardiovascular
- Wound assessment
- Pain (acute/chronic) (all patients will have some sort of pain, especially with acute patients, chronic pain with other injuries like back injuries, both can occur together if someone has chronic pain they will also have acute pain after surgery)
preoperative assessments
- medical/surgical/family history
- blood tests/ scans/x-rays
- nutritional/ fluid status
- drugs (OTC/recreational)
alcohol use - respiratory status
- cardiovascular status
- hepatic/ renal function
- past and current medication use
- endocrine function
- allergies
- psychosocial factors
- cultural beliefs
- spiritual beliefs
Returning to the ward from the post anesthetic care unit (PACU)
- Nursing priorities on return to the ward
- Airway- regular observations (patient has just had anastatic important)
- Vitals (EWS score) (determined by EWS but also by protocol on how often you check them)
- Pain (checking in on pain is very important!!! Patients will have pain, well managed pain shouldn’t turn into chronic pain)
- AVPU
- Orientation to time place person (TPP) (medications can make you hallucinate, you can be alert but confused, )
- Nausea and vomiting (anastatic can make you feel sick after, antinausea medication given after surgery they may need more, are you feeling sick at all)
- Wound check for strikethrough (though the dressing) (wound checking important bleeding)
potential complications for surgery. immediate, early, later
- May be general or specific to type of surgery
- Highest incidence of post-op complications is between 1-3 days post op
- Neish things depending on what type of surgery
Immediate complications - Hemorrhage, atelectasis, shock, low urine output
Early complications - Pain, acute confusion syndrome, nausea and vomiting, fever, secondary hemorrhage (bleeding later one days after surgery). DVT, paralytic ileus (ileus of the small intestine stops working, asking if they have passed wind, which determines there is peristalsis), AKI
Later complications - Bowel obstruction due to adhesions, infection, incisional hernia (hernia that is caused by them having to cut through stomach muscle), keloid scar formation (extra scar tissue)
preventing perioperative complication - preoperative
Pre operative (starts from admission, what risks specifically do they have)
- Pre-assessment clinic
- Fitness/risk assessment
- Addressing comorbidities
Continue/stop relevant medication
Preventing perioperative complication - intraoperative
Intra operative
- Correct timely antibiotics
- Cardiovascular optimization (having a close focus on patients cardiovascular status, by monitoring and adequate fluids)
- Specific drugs (I.e. anti-emetics)
preventing perioperative complication - post operative
Post operative
- Enhanced recovery programs (don’t keep patients resting in bed, breathing optimized, walking around, prevents pressure injury, blood flow)
- Analgesia (
- Early mobilization
Regular post op ward rounds regularly being seen by surgical team)
Considerations for the older people - include surgical
Hazards of surgery for the elderly are proportion to
- The number and severity of co-existing health conditions
- The nature and duration of the surgery
The older patient has less physiological reserves than a younger person
- Lower cardiac reserve
- Decreased renal/hepatic function
- Decreased gastrointestinal function
- Sensory limitations
- Dehydration, constipation, malnutrition may be evident
Bariatric considerations
Obesity increases the risk and severity of complications
During surgery, fatty tissues are especially susceptible to infection
- Wound dehiscence, deep vein thrombosis when supine, increasing the risk of hypoventilation and postoperative pulmonary complications
- Physical characteristics of short thick necks, large tongues, recessed chins associated with an increased oxygen demand and decreased pulmonary reserves- impedes intubation
- Difficulties associated with positioning, bariatric equipment required
What is homeostasis?
A condition of equilibrium (stability or balance) in the body’s internal environment
It is dynamic
Constant fluctuations of both the internal and external environment
Internal conditions usually vary within a very narrow range (pH blood 7.35-7.45)
Core body Temp
BP/HR/RR
BGL
What are the components of the feedback system?
Stimulus:
Any disruption to a controlled condition
Receptor/sensor:
Monitors the environment and responds to a stimulus
Control centre:
Determines set-point/range to be maintained. Analyses input and determines appropriate response (output).
Effector:
Muscles or glands which bring about a response or effect.
What is the negative feedback system?
Inhibitory, therefore negates a change
Prevent sudden severe changes within the body; reverses or negates original stimulus
Once equilibrium is achieved the response is reduced and the process “shut off”
More common
What is the positive feedback system?
Do not help to maintain equilibrium
Do not oppose a change in internal environment
Enhance and amplifies the effector so the response continues at a faster rate
Only stops when stimulus removed
Less common
What is disease (linked to homeostasis)?
What Is Disease?
Disease is any failure of normal physiological function that leads to negative symptoms.
While disease is often a result of infection or injury, most diseases involve the disruption of normal homeostasis.
Any disease process can lead to an imbalance of HOMEOSTASIS this imbalance is what we see in signs and symptoms.
What is necessary for homeostasis?
Effective receptors
Effective brain function–. control centre
Effective major organs
Skin / Musculoskeletal/ Lungs/ Heart/ kidneys/ Liver/Pancreas
An adequate blood volume
More cardiac specific
Effective blood vessels
An effective cardiac pump
Effective kidney function
What are the types of receptors?
Baroreceptors- pressure
Chemoreceptors-gases/chemical substances
Mechanoreceptors- stretch
Nociceptors- pain
Photoreceptors-light
Thermoreceptors- temperature
Homeostasis sign and symptoms?
The signs and symptoms we see are the result of the body’s way of maintaining HOMEOSTASIS
Therefore normal vital signs=normal homeostasis
Abnormal vital signs=a change in homeostasis, due to an acute situation or chronic disease process
What sign and symptoms will be present in DKA?
Hyperglycaemia
Severe fatigue
Polyuria
Polydipsia
Ketones in urine/pear breath
Increase RR
Acid base balance
pH of blood normal range for homeostasis is :
7.35-7.45 -> slightly alkaline
Discuss chronically high CO2 -> COPD patient may have a ‘normal’ mild respiratory acidosis…..
They have a chronic lung disease that is irreversible/ progressive and incurable
What is a post op haemorrhage?
Bleeding after a surgical procedure. The hemorrhage may occur immediately after the surgery or be delayed. It need not be restricted to the surgical wound.
What is hypovolaemic shock?
Hypovolemic shock is an emergency condition in which severe blood or other fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working.
What medications can worsen a patients potential for a post op haemorrhage?
Warfarin and aspirin
Signs and symptoms of hypovolaemic shock?
Hypotension rt loss of blood volume
Tachycardia rt heart compensation for reduced CO
Grey pallor rt less blood to skin as blood being directed to heart
Excess haemorrhage (inc bleeding)
Acute chest pain due to CAD is caused by what?
Increased myocardial 02 demand and decreased myocardial 02 supply
What is the primary goal in chest pain management?
Open the artery and keep it open
What are the 3 commonly used medications in acute chest pain and management?
GTN, morphine, and aspirin
When giving morphine for acute chest pain, what are three key nursing considerations?
RR under 12, altered level of consciousness, and hypotension
Aspirin is what type of drug?
An antiplatelet
The role of statins in acute chest pain management is what?
To lower total cholesterol / low-density lipid levels
Three medication classes used in the treatment of heart failure are what?
Diuretics, statins and beta blockers
Beta blockers do what?
Slow the HR, lower the BP and reduce the force of contraction.
Ace inhibitors do what?
Promote vasodilation and diuresis, decreasing the workload of the heart.
Diuretics do what?
Increase sodium and water excretion by the kidneys
You are looking after a patient who has recently been diagnosed with asthma. You are the practice nurse responsible for providing an education session. Which of the following best describes the cause of their breathlessness?
A. Bronchospasm, increased mucous production and narrowing of airways
B. Coughing, wheezing and apnoea
C. Narrowing of airways, vasodilation and bronchospasm
D. Tachypnoea, decreased mucus production and bronchodilation
A. Bronchospasm, increased mucous production and narrowing of the airways
Metastasis is defined as what?
A. The process of benign cells migrating to another region
B. Cancer cells moving from their original location to other sites
C. Growing in or penetrating a body cavity
D. The interruption of growth of malignant cells
B. Cancer cells moving from their original location to other sites
A common side effect of chemotherapy includes?
A. Decreased level of consciousness
B. Depression
C. Nausea and vomiting
D. All of the above
C. Nausea and vomiting
You are caring for a patient who has right-sided paralysis and aphasia after an embolic stroke that occurred two days ago. These symptoms indicate that?
A. The damage was probably in both hemispheres of the brain
B. The damage was probably in the left side of his cerebrum probably in the frontal area
C. The damage was probably in the right side of the brain
D. He will probably regain function quickly after this type of injury
B. The damage was probably in the left side of his cerebrum probably in the frontal area
Prolonged hypertension results in the following permanent change in the vascular system:
A. Development of lipid plaques in large veins
B. Recurrent infection in peripheral arteries
C. Damage to the arterial walls
D. Increased systemic vasodilation
C. Damage to the arterial walls
The nurse is concerned that their patient may be developing left sided heart failure. Signs and symptoms of left sided heart failure include:
A. Dyspnoea, orthopnea, and a cough
B. Fatigue, dizziness, and a headache
C. Weakness, palpitations and peripheral oedema
D. Diarrhoea, nausea and vomiting
A. Dyspnea, Orthopnea, and cough
What is the underlying pathophysiology of pneumonia?
An infectious microorganism reaches the alveoli, macrophages become overwhelmed and they signal neutrophils, the neutrophils will engulf the alveoli producing a fibrin rich exudate. This exudate fills infected and neighbouring alveoli causing alveoli to stick together and decrease ventilation. The oedema in the alveoli also increase diffusion distance for gases, impairing gas exchange.
The nurse undertakes the essential assessments of cultural and spiritual needs, family support, falls risk, smoking history, braden scale, and then records vital signs. This patient has pneumonia.
Identify 3 other priority nursing assessments that are specific to your patient during this acute stage and give your rationale.
Assess the patient’s airway through seeing if they are able to speak full sentences, and while doing so watching for WOB and use of accessory muscles
Posterior chest assessment, assessing for dullness on percussion of the lung fields (indicating lung consolidation)
Posterior chest assessment, assessing for bronchial breath sounds on auscultation (Can indicate consolidation)
Based on the following nursing assessments for a patient with pneumonia: Assess patients airway, Posterior chest (percussion), Posterior chest (auscultation)
list 3 priority nursing interventions during the acute phase and provide the rationale for each.
Teach the huff coughing technique to mobilize secretions and expand their lungs to promote ventilation and perfusion.
Encourage fluid intake of 2-3L to thin secretions in the airways and alveoli to aid in the removal of secretions and promote effective gas exchange
Positioning - place the pt in the high fowler’s position as this aids in lung expansion and coughing up of secretions.
For a pt that has pneumonia and has an improved condition what would be two assessments the nurse would perform and what would they expect to find that indicates that their interventions have been effective.
Posterior chest assessment, resonance over the lung fields during percussion
Posterior chest assessment, mostly vesicular sounds heard over the lung fields without adventitious sounds during ascultation
Patient 2, who is Maori, is admitted with a myocardial infarction
State 5 important points that the cardiac rehabilitation nurse would provide education on prior to discharge.
Keep diet low in sodium and reduce fluids to 2L and under
Reduce alcohol, cholesterol and caffeine intake
Reduce levels of stress
Exercise regularly
Smoking cessation
Patient 2, who is Maori, is admitted with a myocardial infarction
The patient tells you that they are upset that the pillow reserved for their head was places on their chair. Discuss the actions you would take to ensure that tikanga is observed.
I would apologise that this occurred and ensure the pillows for this patients head were a blue colour to indicate these were for the head and and inform other staff to please keep these pillows at the top of the bed only to ensure the head is respected. Use white pillows for the body. As per tikanga policy
Patient 4, develops pain and swelling in their L) leg. An ultrasound scan confirms a deep vein thrombosis (DVT).
Please outline the aetiology and pathophysiological process that has most likely occurred in the formation of their DVT
DVT’s are caused by 3 main factors described as Virchows triad. These are stasis of blood flow, hyper coagulability, Endothelial injury. You can be more predisposed to these 3 factors if you are older, pregnant, or have had a long period of immobility.
A DVT is a formation of a clot in the deep veins. It is a type of VTE (venous thrombo embolism), blood stasis leads to the formation of a DVT as blood in the peripheral veins will start to clot together due to lack of mobility, hypercoagubility will increase hemostasis of blood in the peripheral veins increasing blood clotting and endothelial damage will causing blood clotting in order to ‘heal’ the damage. This is a result of the platelets in the blood and exacerbated by WBC’s.
You are allocated Patient 5 who was admitted with a spinal fracture at the level of the first thoracic vertebrae (T1) the nurse notices a kink in the patients indwelling catheter
Briefly explain the life-threatening complication that could occur from this, and list the clinical manifestations of this complication that is unique to spinal patients.
This can lead to autonomic dysreflexia as the kinked indwelling catheter can cause bladder distension causing a stimulus in the lower body that the body overreacts to. This will cause symptoms such as HTN, a pale, cool and clammy tone to the lower skin, and flushed upper skin, nausea and vomiting, headache, pupil constriction, and bradycardia. This is unique to spinal patients, particularly those with a spinal injury at T6 or above.
Name three medication commonly used in management of chest pain and their classes and actions
GTN to relax smooth muscle, and dilate veins and arteries
Morphine (analgesia) to depress the CNS hence reduce pain and promote vasodilation
Aspirin (antiplatelet) to impede clotting
Explain the role of statins in acute chest pain management
Statins work to decrease total cholesterol levels which is a risk factor for atherosclerosis. Statins also slow down the progression of disease so they can help delay symptoms such as angina (chest discomfort or breathlessness)
List the three key medication classes in the management of heart failure and give examples of these
Ace inhibitors to promote vasodilation and diuresis by decreasing afterload and preload hence decreasing workload of the heart
Beta blockers to slow conduction (HR) and lessen the force of contraction to reduce myocardial workload
Diuretics to provide relief of clinical symptoms of fluid overload.
What is CAD? other name is…
Coronary artery disease (CAD), also called ischaemic heart disease, happens when the major blood vessels in the heart get narrow and stiff. It can cause myocardial infarction and angina.
What is rheumatic fever?
Rheumatic fever starts with a sore throat that is known as ‘strep throat’ – a throat infection caused by a bacteria called Group A Streptococcus.
This is an autoimmune disease. It happens when your immune system makes a mistake and attacks other parts of your body, as well as the strep throat germs.
This can cause inflammation and oedema in the heart, joints (elbows and knees), brain and skin
Identify signs and symptoms of a person experiencing an arrythmia
Anxiety.
Fatigue.
Lightheadedness or dizziness.
Sweating.
Fainting (syncope) or near fainting.
Monro-Kellie hypothesis states…
that the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.
Define Cardiovascular disease
Any condition that affects the structure and function of the heart and blood vessels
What are some examples of cardiovascular disease?
Coronary Artery Disease (CAD) - Angina, myocardial infarction
Cerebrovascular disease (CVD)
Peripheral vascular disease (PVD)
Heart Failure (HF)
Hypertension
Rheumatic Heart Disease
Congenital Heart Disease
What is Rheumatic Fever?
Autoimmune disease that results from a Group A Streptococcus (GAS) infection in the throat
Is linked to poor housing conditions, overcrowding, socioeconomic deprivation, barriers to primary health care access and a lack of treatment for strep throat
Is largely unseen in the developed world but NZ has one of the highest rates in the world - mainly in the North Island
If untreated, it may develop into rheumatic heart disease and go on to damage the heart - valve/s may need to be replaced
92% of all cases of rheumatic fever affect Māori and pacific island children and young people (aged 4-19)
Define Ischaemic Heart Disease
The term is given to heart problems caused by narrowed heart arteries. When arteries are narrowed, less blood and oxygen reach the heart muscle. Ischemia occurs when there is insufficient blood flow and blood volume to supply the O2 needs of the myocardium
What is the underlying pathophysiology of Ischaemic Heart Disease?
Usually atherosclerosis
What is Angina?
Symptom of reversible myocardial ischaemia
Usually predictable and manageable
Occurs due to a stable lesion/plaque in the coronary artery
A type of chest pain caused by reduced blood flow to the heart (often described as squeezing, pressure, heaviness, tightness or pain in the chest)
What is the key pathophysiology of IHD?
Ineffective myocardial oxygen perfusion
-Myocardial oxygen demand is greater than oxygen supply
-At risk of heart muscle damage/necrosis
-Damaged muscle behaves ineffectively
-At risk of arrhythmia (damaged muscle does not convey impulses well)
-May lead to cardiac arrest
What is a Myocardial Infarction and its characteristics?
-Results from sustained ischaemia or sudden complete blockage of the coronary artery from plaques (atherosclerosis). -If the plaques rupture, you can have a heart attack (myocardial infarction)
-Myocardial tissue distal to the obstruction dies
-Can be partial thickness (NSTEMI) or full thickness (transmural) (STEMI)
-Life-threatening
-Complications include:
Cardiogenic shock, heart failure, ventricular fibrillation (VF) which can lead to death
Definition of an MI - two types
-Non-ST-Elevation Myocardial Infarction (NSTEMI) involves partial thickness myocardial wall damage
-ST-Elevation Myocardial Infarction (STEMI) involves full thickness myocardial wall damage (with/without necrosis)
Compare STEMI and NSTEMI together
Stemi:
-Full thickness damage to the myocardium (transmural)
-Sudden complete blockage of a coronary artery
-ST segment evaluation on an
-ECG
-No need to wait for bloods
-ECG finding is definitive
NSTEMI:
-Partial thickness damage to the myocardium
-Partial blockage of a coronary artery
-Not visible on an ECG
-Need bloods for cardiac biomarkers to diagnose
What is Acute Coronary Syndrome (ACS)?
-Group of clinical symptoms that are consistent with acute myocardial ischaemia. Unless interventions are applied promptly ACS can result in myocardial death
-ACS is the term for an imbalance of 02 supply and demand. The underlying pathophysiology is atherosclerosis which can lead to plaque rupture and thrombus formation
What conditions fall under Acute Coronary Syndrome?
Unstable angina (UA),
Non—ST-segment elevation myocardial infarction (NSTEMI),
ST-segment elevation myocardial infarction (STEMI)
What are some Signs and symptoms of IHD & ACS?
Pale, grey, confused, tachycardic, hypotensive, hypertensive, chest pain, dyspnoea, weak thready pulse, feeling of impending doom, think it’s indigestion, feel like an elephant on their chest, tachypnoeic, fatigue, anxiety, ECG abnormalities, pain radiating across the chest, down the left arm, into the jaw, into the back, palpitations, restlessness, tightness in chest, hypoxaemia, diaphoresis, cyanosis, dizzy, light-headed, nausea
How does the body minimise the effects of an MI?
In absence of O2, cell function will deteriorate:
-Ischaemia: Lack of O2
-Injury: Potentially reversible damage
-Infarction: Necrosis - permanent damage
How is ACS/MI diagnosed?
History (chest pain and related symptoms)
12 Lead ECG (ST elevation height and area of the heart)
Blood tests
Other Diagnostic Investigations that may be Untaken Include::
Coronary angiogram +/- Angioplasty
Echocardiography (ECHO)
Transoesophageal Echocardiography
Exercise tolerance test (ETT)
Electrophysiological studies (EPS)
Chest X-Ray
What are some blood tests that might be used for the diagnosis of ACS?MI?
Troponin T and I - Cardiac specific enzymes
Cardiac enzymes: Creatinine kinase (CK-MB) - mainly in cardiac muscle, myoglobin -
cardiac and skeletal muscle
Electrolytes - K+, NA+, important for electrical conduction and kidney function
Complete blood count (CBC)
Lipid Profile - fasting
Brain Naturide Peptide (BNP)
What is the underlying pathophysiology for ACS?
Group of clinical symptoms that are consistent with acute myocardial ischaemia. Unless interventions are applied promptly ACS can result in myocardial death
ACS is the term for an imbalance of O2 supply & demand. The underlying pathophysiology is atherosclerosis which can lead to plaque rupture and thrombus formation
Unstable Angina Pectoris
STEMI
Non-STEMI
What are precipitants of angina/ACS?
Exercise/ Exertion
↑ HR, ↑ CO, ↑ myocardial O2 demand
Extremes of temperature
Vasoconstriction ↑resistance
vasodilation ↓venous return
Eating a heavy meal
↑ parasympathetic stimulation – blood diverted to the GI system
Emotions/stress
↑ HR, ↑ CO, ↑ myocardial O2 demand
Effects of drugs
Can ↑ or ↓ HR, BP
What are some intervention of ACS?
Follow the Heart Foundation Angina Action Plan (copy on Moodle)
Percutaneous Coronary Intervention (PCI) – the gold standard (watch the YouTube clip on Moodle)
Thrombolysis - fibrinolytic therapy (dissolves clots)
- Alteplase / Metalyse
- Streptokinase
- Tissue plasminogen activator (TPA)
What is the difference between Heart attack and Cardiac Arrest?
Heart attack is a MI
Results from a blocked coronary artery
This prevents oxygen-rich blood from reaching the myocardium
Without oxygen the myocardial cells begin to die
A circulation problem
Cardiac arrest a sudden, cessation of the heart’s functioning
Triggered by electrical malfunction in the heart that causes an arrhythmia (irregular heart beat)
Disrupts the pumping action
An electrical problem
What are the priority goals in management? MI
OPEN THE ARTERY AND KEEP IT OPEN
Increase oxygen supply to the myocardium → give nitrates and consider O2 if SaO2 < 93%
Relieve pain, reduce O2 demand & signs of ischaemia
Preserve viable myocytes
Relieve obstruction:
- Manage thrombus to reperfuse the artery & minimise permanent damage
What are the common cardiac medications?
Aspirin
Metoprolol
Atorvastatin
Cilazapril
GTN spray
What are the different types of cardiac rhythms?
Normal Sinus Rhythm
Arrhythmias
Asystole
Atrial Fibrillation
Name 2 different types of Arrhythmias
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
What is Ventricular Tachycardia (VT)?
Ventricular Tachycardia (VT) is characterised by an absence of P waves as the ventricles have taken over - QRS complex is wide and fast
There is initially a pulse, but VT can progress onto no palpable pulse (no cardiac output) = cardiac arrest (needs defibrillation)
This is a life-threatening rhythm
What is Ventricular Fibrillation (VF)?
Ventricular fibrillation (VF) is characterised by rapid disorganised contraction of the ventricles = life-threatening rhythm - needs defibrillating immediately!!
No discernible atrial or ventricular activity
No palpable pulse (no cardiac output) or respirations = cardiac arrest
VF is the most common arrhythmia in patients with cardiac arrest - can be because of myocardial infarction (MI)
What is Asystole?
Easiest rhythm to memorise
Complete absence of electrical activity - straight line on the monitor
No QRS complexes - no cardiac output
Cessation of the heart’s functioning
What is Atrial Fibrillation (AF)?
Atrial Fibrillation (AF) - completely disorganised atrial electrical activity
Impulses arise from the SA node and other sites in the atria
Conduction through the AV node is irregular and usually fast
There are no P waves and it is irregular
Instead of a P wave - it has uneven fibrillary lines (F waves) before the QRS complex
What are some Atrial Fibrillation Risk Factors?
Older age
Male gender
Obesity
Hypertension
Excessive alcohol intake
Heart Failure
What are some signs and symptoms of Atrial Fibrillation?
SOB
Fatigue
Palpitations
Chest pain
Haemodynamic instability (abnormal or unstable blood pressure)
What is the treatment for Atrial Fibrillation?
Depends on the cause, severity of symptoms and the pattern
Get the rate down – Beta Blockers
Control the rhythm – medication or cardioversion
Anticoagulation due to the risk of thromboembolism
What is a 12 lead ECG?
A diagnostic tool used to help identify pathological changes associated with Acute coronary syndromes (ACS) such as a myocardial infarction (MI)
Detects the heart’s electrical activity through electrodes attached to the skin and relays them as waveforms for interpretation on graph paper
10 physical leads to attach to the patient showing 12 different views of the heart
Where do the ECG leads go?
- On the 4th intercostal space r of sternum
- L of sternum
- between 2 and 4
- 5th IS mid clav
- level with 4 at l ant axillary line
- level with 5 at mid axil line (mid pit)
Name the landmarks for each ECG lead
V1 should go on the right side of the sternum, where the sternum meets the rib
V2 should go on the left side of the sternum, where the sternum meets the rib
V4 goes on the mid-clavicular line on the 5th intercostal space
V3 goes in the middle of V2 and V4
V5 goes horizontally to V4 on the anterior axillary line which is furthest to the front of the side of the chest wall
V6 goes in the mid axillary line which is on the side, vertical to the armpit
One electrode on each arm
Leg electrodes go somewhere down on the calves or thighs which depends on what kind of access you have to the patient’s lower extremities
What is a localised brain injury?
Coup = direct impact
Contrecoup = secondary damage away from injury site
What is a widespread brain injury?
Diffuse axonal injury(brain stem, closed head injury)coma, mortality 33-50%
What is Hypoxic Brain Injury?
Insufficient oxygen and glucose supply to brain tissue
What is a Hypoxic Brain Injury caused by?
Smoke inhalation
Carbon monoxide poisoning
Cardiac arrest
Strangulation
Drowning
Drug overdose
Traumatic birth
Stroke
Electrocution
Pathophysiology of brain injury
Brain Suffers traumatic injury
Brain swelling or bleeding increased intracranial volume
Rigid cranium allows no room for expansion of contents so intracranial pressure increases
Pressure on blood vessels within the brain causes blood flow to the brain to slow
Cerebral hypoxia and ischaemia occur
Intracranial pressure continues to rise. Brain may herniate.
Cerebral blood flow ceases
What damage to the brainstem cause?
Loss of consciousness
Interruption of normal breathing
Interruption of cardiac function
Fixed dilated pupils
What are some contributing factors to gastrointestinal tract conditions?
Bleeding, trauma, perforation, obstruction
Inflammation, infections, infestations
Tumours; benign and malignant
Congenital disorders
Circulatory and nervous system faults
Ageing
High levels of stress and anxiety
Irregular eating habits
Low fibre and water intake
Low levels daily exercise
Congenital /genetic influences
What are the signs and symptoms of Gastrointestinal disease?
Change in appetite
*Weight gain or loss
*Dysphagia
*Intolerance to certain foods
*Nausea and vomiting
Change in bowel habits
Abdominal pain
Flatus
These are sometimes ignored, not recognised by patients or treated by over the counter (OTC) medications
What is Cholecystitis?
Gall bladder inflammation
Associated with:
A mixture of particulate solids precipitated from bile. Consists of cholesterol crystals, calcium bilirubinate pigment, and other calcium salts.
Gallstones (may be asymptomatic)
Incidence higher in females >40yrs
Acute cholecystitis:
Pain + rigidity of upper abdomen
pain radiates to mid sternum or right shoulder region
Associated with nausea and vomiting.
If the common bile duct becomes obstructed = jaundice (yellow tinge to the skin associated with itchiness)
What are the causes of Constipation?
Colonic disorders e.g. volvulus, irritable bowel syndrome (IBS), diverticular disease
Drug induced e.g. antacids, barium sulphate, laxative abuse, opioids, antidepressants.
Opioid induced constipation is a significant issue for post surgical patients.
Management includes regular aperients(prescribed) avoiding use of other constipating medications. Mobilisation and fluids.(Brown, Edwards, Seaton & Buckley,2015 pg. 65)
Systemic disorders e.g. diabetes, spinal cord lesions, stroke
Pregnancy
What is Appendicitis?
Results from kinking or occlusion by faecalith.(hardened mass of faecal matter)
Pain periumbilical progressing to RT lower quadrant at McBurney’s point
Rebound tenderness on palpation
Low grade fever/nausea vomiting
Complications
Peritonitis or localised abscess can occur within 24 hours after onset of pain
What is Irritable Bowel Syndrome?
Results from functional disorder of intestinal motility
Symptoms are present for at least 3 days a month
Chronic intermittent & recurrent abdominal pain
Irregular bowel habit
Diarrhoea, constipation, abdominal distension, flatulence, bloating
Continual defecation urge, urgency, feeling of incomplete evacuation
What is Crohns Disease?
Crohn’s disease:
Common in young adults and adolescents. More common in women and older population (50-80 years).(Farrell,M (2017 p 1011)
Subacute ,chronic inflammation of all layers of colon(transmural)
Oedema and thickening progressing to ulceration of mucosa
Skip lesions separated by normal tissue
Scar tissue and formation of granulomas interfere with normal colon function
What is Ulcerative Colitis?
More common in Caucasian and people of Jewish descent. Peak incidence between 30-50 years 5% patients may go on to develop colon cancer. (Farrell,M ,2017, p 1013)
Affects superficial mucosa rectum and colon
Multiple ulcerations, desquamation of epithelium,
Abscesses form infiltrating submucosa layers
Bowel narrows, shortens presence of fistulas
What are the signs and symptoms of inflammatory bowel disease?
Common for both conditions:
Abdominal pain – usually mild – moderate (Crohn’s) onset in right lower quadrant
Diarrhoea
Bloody stools (more likely with UC)
Weight loss (Crohn’s)
Fever (UC during acute attacks. Common with Chron’s)
Fatigue
Malabsorption
What are the two inflammatory bowel diseases?
Crohn’s disease and Ulcerative colitis
What is the treatment for inflammatory bowel diseases?
Rest the bowel, control inflammation, combat infection, correct malnutrition, alleviate stress, symptomatic relief
Medications
Surgery – 75% of Crohns require surgical intervention either stricturoplasty or resection +/- temp ostomy or ileostomy
Nutritional therapy - according to triggers, malnutrition etc +/- TPN
Some people with IBD suffer extra-intestinal manifestations of disease including arthritis, ankylosing spondylitis, eye inflammation and skin lesions thought to be cause by circulation products of inflammation triggering inflammation in other areas.
What is Volvulus?
Latin word - rolled up, twisted
Twisting of part of intestine around itself = obstruction
Frequently in colon, but can occur in stomach and small bowel
Can lead to: gangrene, obstruction, perforation, peritonitis & death
What are risk factors for colorectal cancer?
Gender ↑males
Age > 55
Family history, familial adenomatous polyposis (FAP)
Colorectal polyps
Inflammatory bowel disease (IBD)
Obesity
Smoking
Excess alcohol consumption
High fat diet
Low fibre diet
What are the tests leading up to a disgnosis of CA Bowel (cancer)
Biopsy from colonoscopy – histology report and mass visualised
CEA( carcinoembryonic antigen) elevated readings.
Abnormal blood results
Mass visualised on CT scan
Palpable mass felt during abdominal examination.
AFTER DIAGNOSIS
Staging /classification of colorectal cancer dictates the management.
Surgery required to remove tumour and part of bowel e.g. hemicolectomy. Abdominal-perineal resection. Laparoscopic colectomy.
May require chemotherapy , radiotherapy, biological and targeted therapy.
What is Colorectal Surgery - Colectomy?
Partial removal of the colon or removal of the entire colon is one of the most common forms of colorectal surgery
The name of the procedure describes the extent of the surgery e.g. hemicolectomy - part of the ascending or descending colon
What is a left hemi colectomy?
Removal of diseased area of bowel and length of normal bowel either side of it.
Removal of any potentially diseased areas.
Two ends of healthy bowel are anastomosed (joined together by stitching or stapling the ends together).
Wound closed with clips or stitches.
Commonly performed laparoscopically or may start this way and proceed to open surgery.
+/- stoma / ostomy (ileostomy, transverse, sigmoid)
Temporary – loop, double barrelled, Hartman’s pouch
Permanent – rectal
What is the nursing management for Colorectal Surgery - Colectomy?
Haemodynamic stability
Pain Control
Fluid & electrolyte balance
Number & appearance stools
Bristol Stool Chart
Wound care
Nutrition status
Skin integrity
Education
-Identifies coping patterns
-Lifestyle modification
Rest versus exercise
Knowledge of disease
Signs & symptoms to prevent complications
What is a Ostomy?
An ostomy is a surgical opening that connects an organ or underlying structure directly to the skin.
There are different types of ostomies created for different purposes to maintain normal body function. They are named after the organ or structure they connect to. e.g.
Tracheostomy is an opening through the neck connecting the trachea allowing the patient to breathe.
What is a Stoma?
A stoma (Greek word for mouth or opening).
The end of the organ or structure on the skin surface.
What is a stoma colostomy?
Part of the colon is brought through the surface of the skin through an opening on to the abdomen.
The output from a stoma is related to the location of the stoma.
Normal bowel habits can be generated with colostomies.
Stools are formed if the stoma is functioning correctly.
They are they are usually active from as frequently as twice a day to as infrequently as second daily.
Usually located on the transverse or descending colon.
May be permanent or temporary (reversible).
What are the Genito-Urinary Stomas?
UROSTOMY - Permanent diversion of the urinary tract involving a stoma.
Common indications include: bladder cancer, urinary incontinence,
congenital abnormalities, interstitial cystitis.
ILEAL CONDUIT- most common type of urostomy
the ureter is implanted into a segment of the ileum
that is led out through the abdominal wall. The
loop of ileum is a passageway for the urine to
pass (sometimes the sigmoid colon is used).
UTEROSTOMY - More common in paediatrics
the ureter is brought to surface of the abdomen
creating the stoma on the surface
What is the Colostomy and Ileostomy formation?
Techniques used:
Terminal or end formation (Colostomy or Ileostomy)
Following a bowel resection. The section of bowel that remains attached to the upper GI tract is brought out onto the abdominal surface. The stoma is created by folding the intestine back onto itself and suturing the end to the abdomen. The other end of the colon is either removed or over sewn. It may be temporary
Specific Indications:
Colostomy - cancer sigmoid colon, inflammatory
bowel disease, diverticulitis, trauma, volvulus,
May be created to rest a portion of bowel.
Ileostomy - When removal of the colon
is required, most commonly for inflammatory
bowel disease.
What is the Preoperative nursing care for stoma surgery?
Management:
Physical:
Manage pain,
Replace fluid & electrolytes
Administer prescribed medications e.g. antibiotics,
Physically prep the patient for surgery (may require bowel prep)
Psychological & emotional support:
Listen to the patients/ family whānau concerns
provide a safe environment and offer opportunities for discussion.
Identify the patients support systems
Offer a visit from a person who has a stoma
Offer to be present when the stoma is first viewed
What is the pre-op education for stoma surgery?
What to expect post op
What to expect for pain management
What to expect with bowel/bladder function
Introduce the patient to the types of appliances and how to fit them.
How to clean their stoma
Diet changes that they may have to make
What are the post operative nursing assessments for stoma surgery?
Colour (beware of the dusky stoma)
should be red / pink
Output
type, colour, consistency
Shape, (spout & size)
Note changes in size particularly if it increases in size
Surrounding skin
condition of skin, redness, ulceration etc
If rod or bridge is in place
Note the position of the rod and if it is holding the stoma in place
Sutures
loose, detached, signs of infection
What is the post operative management for stoma surgery?
Ongoing assessment for post op complications/ report changes
Stoma Nurse specialist consult
Medical team review if problems develop
Good skin care
Appliance review
Stoma output, medication and diet review
Assess and manage fluid and electrolyte balance
Education and support)
Listen to the patient regarding their feelings about their altered body image
Support groups
Asthma: definition
A respiratory condition whereby the airway may tighten, partially close, swell and make more mucus when faced with certain triggers. this causes difficulty breathing.
Asthma: aetiology
is thought to be caused by a combination of genetic and environmental factors. this included
- exercise- induced asthma, can worsen when air is cold or dry
- occupational asthma, triggered by workplace irritants such as chemicals, fumes, gases or dust
- allergy-induced asthma, triggered by airborne substances such as pollen, smoke, tobacco, pet fur.
Asthma: pathophysiology
an inflammatory response is triggered by allergens= mucous secretion that occludes small airways and causes bronchial hyperreactivity
airway inflammation = swelling or oedema of the membranes that line the bronchi and bronchioles
mast cells, when activated, release chemical called mediators which cause inflammatory response, leading to an increased blood flow and movement of white blood cells to the area and bronchoconstriction.
alveoli in areas distal to airway obstruction become hyper-inflated
air trapping within the alveoli causes increased pressure that decreases alveolar perfusion causing a ventilation/ perfusion (V/Q) mismatch. this will initially cause hypoxaemia and eventually cause hypercapnia leading to asthma symptoms.
Asthma: interventions/ assessments
bronchodilators through nebuliser or spacer
administer 02 as prescribed
sit patient upright
reassurance
education
mobilise/ rest as tolerated
monitor sputum.
posterior chest
peak flow
COPD: definition
A group of lung diseases that block airflow and make it difficult to breathe.
Emphysema
Chronic Bronchitis
COPD: signs and symptoms
SOBE
increased RR
decreased SP02
increased HR
fever
chills
Wheeze
Crackles on inspiration
Cough
dullness on percussion
chronic cough
fatigue
sputum production
increased frequency of chest infections
tripod positioning
clammy skin/ diaphoresis
dizziness
COPD: assessment/ interventions
encourage fluids to moisten secretions
position upright to maximise air entry
educate breathing techniques. pursed lip breathing, exhalation of c02
bronchodilators
ABS
COPD: pathophysiology
tobacco smoke/ air pollution causes
inflammation of the airway epithelium, which leads to
infiltration of inflammatory cells and release of cytokines, which can cause
systemic effects (muscle weakening and loss)
this can lead to continuous bronchial irritation and inflammation
- chronic bronchitis (bronchial oedema, hypersecretion of mucus, bacteria; colonisation of airways
or
breakdown in lung elastic tissue
- Emphysema (destruction of alveolar septa and loss of elastic recoil of bronchial walls)
both of which can result in
- airway obstruction, air trapping, loss of surface area for gas exchange, frequent exacerbations (infection, bronchospasm), Evident by Dyspnea, cough, hypoxemia, hypercapnia or pulmonia.
.
.
Pneumonia: signs and symptoms
SOBE
increased RR
decreased SP02
increased HR
fever
chills
Wheeze
Crackles on inspiration
Cough
dullness on percussion
Pneumonia:
acute infection of the lung parenchyma
Pneumonia: Assessments/ interventions
administer ABs
encourage fluid intake, IV fluids
encourage coughing technique
position upright
cooling cares
educate good hand hygiene.
Pneumonia: pathophysiology
- bacteria invades spaced between cells and alveoli
- inflammatory response + alveolar macrophages try to control infection
- fluid and mucus buildup in lungs
- impaired gas exchange and circulation
- ventilation exceeds pulmonary perfusion (V/Q) mismatch.
influenza: definition
influenza is an acute inflammation of nasopharynx, trachea and bronchioles with congestion, oedema and the possibility of necrosis of respiratory structures.
influenza: signs and symptoms
fever
cough
sore throat
runny/ stuffy nose
body aches
headaches
chills
upset stomach
influenza: pathophysiology
- virus enters the respiratory tract attaching to epithelial cells
- enters host cell and uses host DNA to replicate the disease
- new viral spores are released from host cell
- destruction/ desquamation of trachea and bronchi means on basal layer of epithelium remains
- damage to epithelial cell wall causes oedema and possibly haemorrhage of submucosa leading to cell death
- necrotic cells may undergo phagocytosis by macrophages, recruiting neutrophils
- results in alveolar wall oedema causing ineffective gas exchange.
influenza: aetiology
there are age groups more susceptible to influenza including
- elderly
- young children and pregnant women
- adults and children with chronic disorders of pulmonary and or circulatory systems
- those living in nursing homes or long term care.
influenza: assessments and interventions
administer bronchodilators
encourage fluids
cooling cares
educate hand hygiene
prevention (immunisation)
pulmonary embolism: definition
is a blockage in one of the pulmonary arteries in the lungs
pulmonary embolism: signs and symptom
SOB
chest pain
cough
increased HR or palpitations
decreased SP02
pulmonary embolism: Aetiology
a pulmonary embolism is caused by blood clots that travel from the legs, or rarey other parts of the body. (DVT deep vein thrombosis)
risk factors include
- conditions and disorders that blood clotting as a result of venous stasis
- decreased mobility
- hypercoagulability
- pregnancy and injury to endothelial cells that line vessel
- no matter the source, a blood clot becomes an embolus when all or part of it breaks away from the site of formation into the bloodstream
pulmonary embolism: assessments/ interventions
administer anticoagulants
encourage regular mobilisation and position changes
reassure and educate about PE treatment options
administer 02 as required.
ischaemic heart disease: definition
increases myocardial oxygen demand and decreased myocardial oxygen delivery results in ineffective myocardial oxygen perfusion
ischaemic heart disease: signs and symptoms
can range from no symptoms, to chest pain, to a heart attack.
ischaemic heart disease: pathophysiology
- atherosclerosis leads to heart damage and necrosis of the myocardium
- heart damage leads to cardiac arrest/ arrhythmias.
ischaemic heart disease: aetiology
coronary artery disease (CAD) is the most common type of heart disease and happens with the arteries that supply blood to the heart muscle (coronary artery) become hardened and narrowed.
- A gradual blockage can result in angina.
- A sudden or severe blockage can result in heart attack or cardiac arrest.
Risk factors
- HTN
- smoking
- diabetes
- high fat and cholesterol diet
ischaemic heart disease: assessments and interventions
lifestyle changes, medications, angioplasty and surgery.
physical exercise, smoking cessation, weight loss, low fat diet
GTN spray
medications
- statin (decreased liver’s production of harmful cholesterol)
- blood thinners (helps prevent blood clots from forming, dissolves old ones)
- beta blockers (slows heart rate and decreases blood pressure)
- calcium channel blockers (relaxes blood vessels)
- heart medications (helps reduce chest pain or pressure caused by blockage in arteries of heart)
coronary stent
- tube placed in the arteries of the heart to keep them open
coronary angioplasty
- unblocking an artery by inflating a balloon inside it. A stent may also be inserted to hold artery open
coronary artery bypass surgery.
Atherosclerosis: definition
the build up of fats, cholesterol and other substances in and on the artery walls.
Atherosclerosis: signs and symptoms
Atherosclerosis often has no symptoms until a plaque ruptures or the build up is severe enough to block blood flow.
- chest pain.
- SOB
- Fatigue
- tightening of the chest
Atherosclerosis: pathophysiology
- an irritant is present, e.g. lipids, high blood pressure, toxins, diabetes.
- damage occurs to the endothelium by the irritant- a crack of fissure is formed.
- LDL cholesterol deposits accumulate in the artery wall known as fatty streaks
- LDL oxidases and sends signals to the immune system and monocytes (WBC) arrive
- monocytes convert to macrophages and consume the cholesterol
- macrophages fill up on cholesterol and die = foam cells
- formation of foam cells = release of cytokines
- smooth muscle cells migrate into expanding fatty plaque forming a lipid cap
- smooth muscle cells also deposit calcium into the fatty plaque, hardening it and causing bulging into the artery lumen
- blood flow is decreased(resistance increased)and compliance is reduced (less flexibility)
- ongoing inflammation= plaque rupture, thermogenic material inside cap is exposed= arriving platelets from a thrombus
- a thrombus is formed and occludes the artery causing ischemia or infarction
Atherosclerosis: aetiology
high blood pressure
high cholesterol
high triglycerides
smoking and or sources or tobacco
insulin resistance, obesity or diabetes
inflammation from diseases such as arthritis, lupus or infections or inflammation of unknown cause.
Heart failure: definition
is the heart’s inability to consistently pump enough blood to organs and tissues.
Heart failure: pathophysiology
- MI or cardiac dysfunction / structural abnormality impairs ability of the left ventricle to fill with or eject blood
- poor ventricular function/ myocardial damage leads to decreased stroke volume and cardiac output
- leads to a neurohormonal response
- either sympathetic system activated to increase cardiac workload or RAAS cc c pathways activated
- results in vasoconstriction and sodium + fluid retention
- further stress on the ventricular wall and remodeling leads to heart failure.
Heart failure: aetiology
commonly caused by IHD (decreased contraction, ventricular filling or both). more common among the elderly.
can be caused by AF, HTN, diabetes smoking, drinking excessively , HIV and some cytotoxic drugs.
Heart failure: assessment and intervention
ensure daily weights
start FBC and fluid restrictions
educate on healthy eating and exercise
furosemide?
Chronic renal failure/ kidney injury: definition
progressive irreversible loss of kidney function and decreased GFR for at least three months.
can lead to AKI, interventions aim to prevent AKI
Chronic renal failure/ kidney injury: signs and symptoms
Nausea
Vomiting
Loss of appetite
Fatigue and weakness
Sleep problems
Urinating more or less
Decreased mental sharpness
Muscle cramps
Swelling of feet and ankles
Dry, itchy skin
High blood pressure (hypertension) that’s difficult to control
Shortness of breath, if fluid builds up in the lungs
Chest pain, if fluid builds up around the lining of the heart
Chronic renal failure/ kidney injury: pathophysiology
.
Chronic renal failure/ kidney injury: aetiology
At the early stages people have no symptoms:
Diabetes
Hypertension
Smoking
Obesity
Ethnicity
Gender men>women
Age - kidney function decreases with age
Specific conditions – glomerulonephritis
Chronic renal failure/ kidney injury: assessments and interventions
Nursing interventions:
Maintain adequate nutrition
Fluid restriction
Promote activity & rest as tolerated
Provide skin care
Provide education on condition & complications
Provide culturally appropriate care
Psychological/emotional l support
Support for smoking cessation
Acute kidney failure/ kidney injury: definition
Acute kidney injury (AKI)occurs when the kidneys are unable to remove the body’s metabolic waste or perform their seven regulatory functions – in particular, for cardiac week - maintenance of BP and electrolyte regulation
Acute kidney failure/ kidney injury: signs and symptoms
passing less urine (pee) than usual
very concentrated urine, or urine looking yellow/brown/red in colour
loss of appetite
nausea or vomiting
fatigue and short of breath
feeling confused, anxious and restless, or sleepy
swelling of legs or other body parts
pain in abdomen or lower back.
Acute kidney failure/ kidney injury: pathophysiology
.
Acute kidney failure/ kidney injury: assessment and intervention
Assessments:
Fluid balance chart (FBC)
Daily weigh (1kg of weight = 1L retained fluid)
Skin integrity
Vital signs → EWS
Capillary refill time (CRT)
Palpate and/or scan the bladder
Bloods – GFR, electrolytes, CBC
Ability to manage ADLs
DVT: signs and symptoms
throbbing pain in 1 leg (rarely both legs), usually in the calf or thigh, when walking or standing up
swelling in 1 leg (rarely both legs)
warm skin around the painful area
red or darkened skin around the painful area – this may be harder to see on brown or black skin
swollen veins that are hard or sore when you touch them
DVT: definition
DVT (deep vein thrombosis) is a blood clot in a vein, usually in the leg.
DVT: pathophysiology
Deep venous thrombosis usually begins in venous valve cusps. Thrombi consist of thrombin, fibrin, and red blood cells with relatively few platelets (red thrombi); without treatment, thrombi may propagate proximally or travel to the lungs.
- Decreased or mechanically altered blood flow
- Trauma to blood vessels stimulates the clotting cascade
- Platelets aggregate at the site, especially where venous statis is present
- Platelets and Fibrin form the initial clot
- Decreased blood flow leads to decreased oxygenation and increase in hematocrit (increase in RBC in the blood volume)
- RBC are trapped in the fibrin meshwork
- Clot may completely occlude blood vessel or embolus may travel to other parts of the body (lungs or brain).
DVT: Virchow’s triad
Virchow’s Triad distills the multitude of risk factors for DVT into three basic elements favouring thrombus formation: venous stasis, vascular injury and hyper coagulability.
Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT.
Paralytic ileus: definition
The condition where the motor activity of the bowel is impaired, usually without the presence of a physical obstruction.
Paralytic ileus: signs and symptoms
Abdominal bloating, abdominal distension, Gas, Constipation, Nausea and vomiting, dehydration.
Paralytic ileus: pathophysiology
Paralytic ileus occurs when the muscle contractions that move food through your intestines (peristalsis) are temporarily paralyzed.
- SNS activated intra operatively and bowel motility inhibited
- Increase in cytokines and inflammatory mediators decrease bowel motility
- Peristalsis slows then stops
- This leads to decreased movement of faecal matter through the bowel
Traumatic brain injury: signs and symptoms
Loss of consciousness from several minutes to hours
Persistant headache or headache that worsens
Repeated vomiting or nausea
Convulsions or seizures
Dilation of one or both pupils
Clear fluids draining from nose and ears
Inability to awaken from sleep
Traumatic brain injury: pathophysiology
Traumatic brain injury occurs when a traumatic event causes that brain to move rapidly within the skull, leading to damage.
Damage of neuronal tissues associated with TBI fall into two categories:
Primary injury, which is directly caused by mechanical forces during initial insult; and secondary injury, which refers to further tissue and cellular damages following primary insult.
Traumatic brain injury: definition
Brain dysfunction caused by an outside force, usually a violent blow to the head.
ischemic/ hemorrhagic stroke: signs and symptoms
Motor deficits – most obvious – include: mobility, respiratory function, swallowing and speech, gag reflex, self care abilities
Hemiplegia (paralysis) / hemiparesis (weakness)
Ataxia = altered coordination of movement & posture (cannot coordinate movement – lost sense of where body part is located, staggering/abnormal walking movements)
Dysphagia = altered swallow
Communication –
Speech = aphasia (inability to use or comprehend words), expressive & receptive dysphasia – depending on area affected these will differ eg – damage to Wernickes area – may have fluent aphasia – faulty understanding of written or spoken words, might produce a string of words with no meaning (word salad), or damage to Brocca area – non fluent – inability to properly form words (know what they want to say but cannot speak the words)
Intellectual Function – Both memory and judgement may be impaired, L side damage more likely to result in memory problems, R side tends to mean pt is impulsive
Spatial perceptual - more common with R side – patients may deny their illness or their body parts. Neglect of one side of body (may be made worse by homonymous hemianopia) , spatial orientation – can’t judge distances, agnosia – cant recognise an object by sight, touch or hearing, and apraxia – inability to carry out learned sequential movements on command
Affect - may have trouble controlling emotions, responses may be exaggerated or unpredictable, depression an issue, frustration, lability
Focus in on terminology
Hemianopia / diplopia
Memory – short & long term affected, low attention & concentration, altered judgement & abstract thought
Emotional lability
Elimination – symptoms more often temporary than permanent but need to consider functional incontinence (resulting from cognitive, functional or environmental factors)
ischemic stroke: pathophysiology
Ischaemic cascade:
- disrupted blood flow
- Anaerobic respiration
- Lactic acid
- Insufficient ATP
Ion imbalance:
- Increase in intracellular calcium
- Increase Glutamate
- Vasoconstriction
Enlarged area of infarction into penumbra:
- Cell membrane and proteins break down
- Formation of free radicals
- Proteins production decreased
- Cell injury and death
hemorrhagic stroke: pathophysiology
Ruptured vessel:
- Explosive eruption of blood from vessel into surrounding brain tissue and structure
- Haematoma develops
- Exposure of brain to blood, an increase in intracranial pressure caused by sudden entry of blood into the tissue, and secondary ischaemia result from reduced blood flow/perfusion.
ion imbalance:
- Mismatch between blood flow and metabolic demand
- Breakdown of sodium/potassium pump maintaining cellular function
- Anaerobic respiration to produce ATP
- Increased production of lactic acid
Cell death:
Altered pH
Cell membrane and proteins break down
- Formation of free radicals
- Cell injury and death
ischemic/ hemorrhagic stroke: aetiology
Modifiable contributing factors:
- High cholesterol
- diabetes
- Obesity
- Inactivity
- Smoking and ETOH
- Hypertension
Non-modifiable contributing factors:
Age
More common in over 55-year-olds
Gender
Women have a higher incidence of stroke than men
Ethnicity
NZ Maori have a greater incidence than non-Maori
Greater incidence in South Asian and African/Caribbean population
Genetics
Small vessel disease in approx. 7% of stroke in young adults
ischemic/ hemorrhagic stroke: assessments and interventions
Nursing interventions:
Maintain head of bed 30◦
to facilitate jugular venous drainage and help reduce intracranial pressure
Maintain systolic blood pressure within prescribed parameters (often < 180mmHg)
to reduce the potential for further bleeding or ischaemic changes
Continuous neurological observations
to help identify deterioration to initiate timely intervention and treatment
Ensure correct positioning of paralysed limbs
to prevent contractures and maximise function for rehabilitation
Ensure patient is kept NBM until swallow is assessed by Speech and Language Therapist
to prevent aspiration of oral fluid and food
Administer prescribed aspirin orally or enterally
to impede clotting and prevent further ischaemia
Turn the patient regularly
to maintain skin integrity and prevent pressure injury if the patient cannot move themselves
Spinal cord injury: definition
A spinal cord injury (SCI) is damage to the tight bundle of cells and nerves that sends and receives signals from the brain to and from the rest of the body.
Spinal cord injury: signs and symptoms
HTN (>20mmHg pt baseline) - Bradycardia
Headaches
Blurred vision
Facial Flushing
Diaphoresis above level of injury
Anxiety and restlessness.
Spinal cord injury: pathophysiology
- Noxious stimulus (distended bladder, constipation etc.)
- Signals transmitted to spinal cord to initiate SN activation (> HR, > BP - vasoconstriction, > RR)
- HTN stimulates baroreceptors in carotid bodies. Brain initiates PN activity to reduce BP by slowing HR (bradycardia)
- Signals to reverse SN activity sent from brain via spinal cord to vasodilate blood vessels, slow HR. This occurs ABOVE SCI level
- Signals cant pass BELOW level of injury. if noxious stimulus continues, ascending signals continue to initiate SN activity.
- Results in increasing HTN (associated headache, blurred vision) bradycardia, vasodilation ABOVE SCI level and vasoconstriction BELOW.
Spinal cord injury: Types of spinal cord injury
Transient concussion (reversible)
Contusion - Bursed
Laceration- Cut to cord
Compression - Squashed cord
Transection (irreversible) - cut straight through spinal cord
Spinal cord injury: assessments and interventions
Interventions:
Put the person into sitting position 90◦ to help lower the BP
Loosen clothing
Assess for the probable cause and remove
Continue to assess vital signs (Q2-3min BP)
Administer GTN as prescribed if SBP > 150mmHg (short acting anti-hypertensive medications only)
Compartment syndrome: Definition
A painful and dangerous condition caused by pressure build-up from internal bleeding or swelling of tissues.
The pressure decreases blood flow, depriving muscles and nerves of required nourishment.
Occurs in long bone fractures.
Compartment syndrome: signs and symptoms
Bulging or visible swelling of the muscle.
Feeling like the muscle is fuller, swollen or somehow larger than normal.
Numbness.
Muscle pain that is stronger than you’d expect from the injury.
Severe pain when you stretch the muscle.
Tightness in the muscle.
Tingling or burning sensation in or under your skin, called paresthesias.
Compartment syndrome: pathophysiology
Fluid enters a fixed volume compartment (eg from bleeding)
Increase in tissue and venous pressure
This pressure exceeds capillary perfusion pressure
Capillaries collapse
Muscle and nerve ischemia occurs
OR…
External compression (eg plaster cast)
Decrease in size of compartment
Increase in intracompartment pressure and decrease in arteriolar pressure
Leads to muscle and nerve ischemia
Compartment syndrome: aetiology
Acute compartment syndrome can also occur after injuries without bone fractures, including:
Crush injuries
Burns
Overly tight bandaging
Prolonged compression of a limb during a period of unconsciousness
Surgery to blood vessels of an arm or leg
A blood clot in a blood vessel in an arm or leg
Extremely vigorous exercise, especially eccentric movements (extension under pressure)
Compartment syndrome: The 5 P’s of neurovascular assessment relating to compartment syndrome
Pain, Pallor (pale appearance), pulselessness, paresthesia (burning or prickling sensation), poikilothermia (temperature control).
Autonomic dysreflexia: definition
Autonomic dysreflexia isan abnormal, overreaction of the involuntary (autonomic) nervous system to stimulation. The most common cause of Autonomic dysreflexia is spinal cord injuries.
Autonomic dysreflexia: signs and symptoms
Hypertension
Bradycardia
Sweating
Flushing
Pupillary constriction
Nasal congestion
Pale cool skin
Piloerection (goose bumps)
Autonomic dysreflexia: aetiology
ingrown toenail, constipation intense pain, kinked catheter, distended bladder, urinary tract infection, pressure injury
Autonomic dysreflexia: pathophysiology
- Strong discomfort/pain stimulus sending signal into spinal cord via intact peripheral nerves below T6 lesion
- CNS senses this input as it travels up the spinal cord evoking a massive Peripheral sympathetic response through spinal reflexes and sends the Sympathetic Nervous System signals and vessels vasoconstrict below the level of the T6 injury
- Vessels continue to constrict as they are trying to send signals to the brain -
peripheral artery hypertension occurs - Brain detects hypertensive crisis through baroreceptors in carotid and aortic arch but CAN’T get the signal to relax vessels and decrease blood pressure into the lower extremities because the spinal cord is severed
- Brain attempts two maneuverers to halt hypertensive crisis
May…
6. Attempts to Shut down sympathetic surge by sending descending inhibitory impulses
Impulses unable to travel to most sympathetic outflow areas due to spinal cord injury at T6 or above
OR….
6. Attempts to decrease peripheral BP by slowing Heart Rate through an intact vagus (parasympathetic) nerve
Compensatory bradycardia is inadequate, and hypertension continues
- Sympathetic nerves prevail below level of spinal injury and parasympathetic nerves prevail above level of injury causing vasodilation above the level of injury (T6) and Vasoconstriction below T6 injury causes increase BP and the vagus nerve causes bradycardia.
- Reflex hypertension eases with removal of noxious stimulus
Myocardial infarction:
A myocardial infarction (commonly called a heart attack) is an extremely dangerous condition that happens because of a lack of blood flow to your heart muscle. The lack of blood flow can occur because of many different factors but is usually related to a blockage in one or more of your heart’s arteries. Without blood flow, the affected heart muscle will begin to die. If blood flow isn’t restored quickly, a heart attack can cause permanent heart damage and death.
myocardial infarction: signs and symptoms
Chest pain (angina). This can be mild and feel like discomfort or heaviness, or it can be severe and feel like crushing pain. It may start in your chest and spread (or radiate) to other areas like your left arm (or both arms), shoulder, neck, jaw, back or down toward your waist.
Shortness of breath or trouble breathing.
Fatigue.
Trouble sleeping (insomnia).
Nausea or stomach discomfort. Heart attacks can often be mistaken for indigestion or heartburn.
Heart palpitations.
Anxiety or a feeling of “impending doom.”
Sweating.
Feeling lightheaded, dizzy or passing out.
myocardial infarction: pathophysiology.
myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a “wavefront” of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart.
myocardial infarction: aetiology
Coronary artery spasm.
Rare medical conditions: An example of this would be any disease that causes unusual narrowing of blood vessels.
Trauma: This includes tears or ruptures in the coronary arteries.
Obstruction that came from somewhere else in your body: A blood clot or air bubble (embolism) that gets trapped in a coronary artery.
Electrolyte imbalance.
Eating disorders: Over time, these can damage your heart and ultimately result in a heart attack.
Takotsubo or stress cardiomyopathy.
Anomalous coronary arteries (a congenital heart defect you’re born with where the coronary arteries are in different positions than normal in your body. Compression of these causes a heart attack).
myocardial infarction: assessments and interventions
Interventions:
Supplemental oxygen
Medications
Education
Angina: definition
a type of chest pain caused by reduced blood flow to the heart
Angina: signs and symptoms
Discomfort, heaviness or tightness of the chest which may spread to the back, shoulders, neck or jaw. Other people describe it as a dull ache
Discomfort in the arm, neck or jaw with no chest discomfort
The discomfort can range from mild or dull to severe.
Angina: aetiology
Angina is usually caused by coronary artery disease (also called atherosclerosis), which is the build-up of plaque in the walls of your arteries
Angina: pathophysiology
Almost invariably, angina is associated with significant obstruction of at least one major coronary artery.
Oxygen demands not met. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands.
Increased demand. When there is an increase in demand, flow through the coronary arteries needs to be increased.
Ischemia. When there is blockage in a coronary artery, flow cannot be increased, and ischemia results which may lead to necrosis or myocardial infarction.
Schematic Diagram for Angina Pectoris via Scribd.
Atelectasis: definition
Partial or complete collapse of a lobe or the entire lung, common post op complication.
Atelectasis: signs and symptoms
Atelectasis often causes no symptoms on its own, though some underlying conditions that lead to atelectasis (like COPD) can cause symptoms.
However symptoms that may be experienced are:
Trouble breathing/shortness of breath (dyspnea).
Coughing.
Chest pain.
Rapid breathing (tachypnea).
Skin and lips turning blue.
Increased HR
Decreased O2
Decreased chest expansion on one or both sides
Atelectasis: pathophysiology
Reduced ventilation or blockage
Obstruction of air to and from alveoli
Trapped air absorbed into bloodstream, blockage stops further air entering alveoli
Area of lung becomes airless
Lung collapse
Respiratory distress
Atelectasis aetiology :
Reduced Alveolar ventilation due to compression or absorption
Trapped 02 is absorbed in the blood stream
No further 02 is absorbed because of blockage
Alveoli collapse leading to acute respiratory distress
Atelectasis: assessments and interventions
Intervention:
Deep breathing exercises
- DBE aim to allow as much oxygen in as possible to increase lung expansion and remove any sputum that may be present. DBE can re-expand the lung tissue such as alveoli that are unable to be inflated correctly during atelectasis.
Nursing actions to prevent atelectasis:
1. Spirometer is used to help the lungs to strengthen by encourage deep, full breaths. The pt aims to breathe in slowly and hold their breath for as long as comfortable. this device should be used at least 10 times every hour to promote recovery.
2. Administer bronchodilators
3. Have pt sitting upright to increase lung expansion and gas exchange
4. Education on breathing techniques and importance of coughing to excrete mucous.
Meningitis: definition
Meningitis: Pathophysiology
There are two types of meningitis, Bacterial and viral.
Bacterial- the entry of bacteria into the cerebrospinal fluid (CSF) and bacterial growth in this compartment leading to inflammation within the CSF and the adjacent brain tissue.
Viral - Once the virus has replicated and caused dysfunction within the immune system, it is able to cross the BBB (Blood-brain barrier) where it enters the cerebrospinal fluid
Meningitis: risk factors
Not having completed childhood vaccinations, Children under the age of 5 years and adults over 50 years, living in overcrowded houses and co morbidities.
Meningitis: Signs and symptoms
Infants and children- Fever, crying, unsettled, irritable, vomiting, sleeping, harder to wake, reluctant to walk, rash
Teens and adults- Fever, Headache, vomiting, sleeping, confusion, delirious, Unconscious, joint pain, aching muscles, stiff neck, photophobia, rash.
Stoma: definition
An opening on the abdomen. connected to either the digestive system or urinary system to allow waste to divert out of the body.
Stoma: colostomy, ileostomy, and urostomy
Colostomy: Opening from the large intestine through the abdomen. can be temporary or permanent. can be located in ascending, transverse, descending, or sigmoid.
Ileostomy: opening in the abdomen wall located on the right lower abdomen, at the end of the ileum.
Urostomy: opening in the abdominal wall. re- directs urines away from the bladder thats diseased or injured.
Stoma: pt education
Pouches needs to be changed every 3-7 days but the pouch needs to be emptied regularly every day to decrease the risk of infections. it can take the stoma a few days to work correctly therefore, slowly introduce foods.
Characteristics and what you are looking for with fluid for a pressure injury?
Is there fluid in the wound? If so, what type?
- An intact or ruptured fluid-filled blister corresponds to a stage 2 pressure injury
- An intact or ruptured blood-filled blister corresponds to a deep tissue pressure injury
Characteristics and what you are looking for with colour for a pressure injury?
What colour is the wound?
Reddened, intact tissue that doesn’t blanch indicates stage 1 pressure injury
Pink or red tissue that’s moist and superficial indicates stage 2 pressure injury
Dark red, purple, or maroon tissue with or without the overlying skin indicates a deep tissue pressure injury
Characteristics and what you are looking for with exposed or directly palpable tissue for a pressure injury?
- What tissues do you see or feel in the wound bed?
- Slough or eschar obscuring the wound bed so that you can’t determine the level of tissue destruction is an unstageable pressure injury
- If adipose tissue is visible in the wound (globular, yellow appearance and/or granulation tissue) then you know it is a stage 3 pressure injury
- Any wound with the deeper tissues exposed or palpable (fascia, muscle, ligament, tendon, cartilage or bone) is a stage 4 pressure injury
What do nurses use to help guide their practice?
Tools
Frameworks
Processes
Policies
Procedures
Best Practice Guidelines
What does ADPIE stand for?
A - Assess
D - Nursing Diagnoses (Identify actual problems and potential problems)
P - Plan care and undertake
I - Intervention (intervene in their care for a better outcome for the patient - sitting them up 90 degrees to increase lung expansion and better breathing)
E - Evaluate care
What does the Health Assessment Framework include?
Psychosocial
Patients account of their history/presentation
Vital signs
Systems review
Subjective (questioning) and objective (physical examination) data
Medications
Discharge planning and ongoing care
Education and health promotion needs
Discharge considerations
Assessment summary
What does COLDSPA stand for?
C - Character (describe…)
O - Onset (When did it begin?)
L - Location (where is it? Does it radiate?)
D - Duration (How long does it last? Does it recur?)
S - Severity (How bad is it?)
P - Pattern (What makes it better or worse?)
A - Associated Factors (What other symptoms occur with it? How does it affect you and every day life?)
What is the Glasgow Coma Scale sections?
Eye Opening Response:
4 - Spontaneous
3 - To Sound
2 - To Pain
1 - Non
Coma: no eye opening
Best Verbal:
5 - Response/Orientation
4 - Confused
3 - Inappropriate words
2 - Incomprehensible sounds
1 - None
Best Motor Response:
6 - Obeys Commands
5 - Localises to stimulus/pain
4 - Withdraws from painful stimulus (flexion)
3 - Abnormal flexion in response to pain (decorticate rigidity)
2 - Abnormal extension in response to pain (decerebrate rigidity)
1 - Flaccid/no response
What is the Glasgow Coma Scale?
The Glasgow Coma Scale is a clinical scale used to reliably measure a person’s level of consciousness after a brain injury. The GCS assesses a person based on their ability to perform eye movements, speak, and move their body.
What is the normal GCS of a person?
GCS 15
What does AVPU stand for?
A - Alert
- The patient is lucid and fully responsive, can answer your questions, can see what you’re
doing
V - Voice
- The patient responds to your voice, but may be drowsy, keeps their eyes closed and may
not speak coherently
P - Pain
- The patient is not alert and does not respond to your voice, but a painful stimulus. EG,
shaking the shoulders or possibly pinching an war lobe, elicits a response
U - Unresponsive
- The patient is unresponsive to any of the above. They are unconscious
(anything other than A, then perform a GCS)
What does ISBAR stand for?
Tool used for handover of information clearly and concisely:
I - Identify S - Situation B - Background A - Assessment R - Request/Recommendations
What are the three principles of acute management?
Correct the Immediate and Life-threatening problems
Treat the cause
Prevent further attacks/episodes/complications
What do you need to be aware of when administering a drug?
Approved Generic name and drug group or category
Monitoring requirements
Patient education
Common adverse effects and how to detect them
Significant drug interactions, contra-indications and precautions
Pharmacodynamics mechanism and site of action
Pharmacokinetics particular parameters and concerns to be aware of
DVT Patho
DVT is formed when red blood cells, fibrin and platelets bind together and create a clot. Increased numbers of fibrin and blood cells build up behind the thrombus and attach to it increasing the size of the clot
What are some nursing interventions for Atherosclerosis?
Administer asprin as prescribed to reduce the ability of the blood to clot and so the blood flows easier through narrowed arteries
Administer oxygen as prescribed to keep Sp02 levels within target and to increase oxygen levels
Reassurance to decrease the SNS response and therefore decrease HR
Educate around stress and relaxation techniques. Stress causes a persistent increase in cortisol levels, which is linked to cardiac function as well as increase adrenaline levels which increases HR and RR.
What are some nursing interventions for DVT?
A
Maintain bed rest to reduce risk of thrombus dislodging
Administer anticoagulants to breakdown clot and prevent further clot formation
Elevate legs above heart to reduce stasis and decrease swelling
Apply TED stockings as prescribed as compression stocking enhance circulation by providing a graduated pressure on the leg to help return the venous blood to the heart
What clinical presentation are we observing for with Neurological changes?
- Anxiety
- Agitation
- Confusion
- Drowsiness
- Pain
What clinical presentations are we observing for with the skin?
- Diaphoresis
- Pallor
- Cyanosis (blue tinge, think about peripheral (capillary refit test.) Looking around the lip,
face and sternum) - Flushing
- Digital clubbing
What are the two types of Bronchodilators: B2-agonists and what does each one do?
- Short-acting (SABAs) = relieve the effects
- Long-acting (LABA) = controllers
How do Short-Acting (SABAs) work?
- Provide relief for 4-6 hours
- Rapid onset of action - 5-10 mins
- Can be used in an acute asthma attack (usually blue inhalers)
How do Long-Acting (LABAs) work?
- Long duration of action (12hrs)
- Slow onset of action
- Not to be used to relieve acute symptoms
What are Inhaled Corticosteroids - ICS (preventers) and how do they work?
- Potent anti-inflammatory agents
- Given via inhalation route greatly reduced systemic adverse effects
- EG. Fluticasone (Flixotide), Beclomethasone (Beclazone)
- Reduce the hyper-responsiveness of the bronchial smooth muscle to irritants
Inhaler VS Spacers VS Nebulisers for Asthma? - What are the differences and how do these work separately?
- INHALER: Pushes out a pre-measured spray of asthma medicine
- SPACER: A spacer is a specially designed plastic tube for use with an inhaler. A spacer used with a puffer delivers more medication into the lungs than using a puffer on it’s own
- NEBULISER: A machine that converts liquid medication into a fine mist, which is inhaled through a mask or mouthpiece
What does poor gas exchange indicate?
Hypercapnia (Greater than normal levels of C02) and Hypoxaemia (Less than normal levels of 02 in the blood)
Effects of Hypercapnia?
- Tachypnoea (Increased Respiratory rate) to “blow off” excess CO2
- Use of accessory muscles to increase chest expansion and help with forced exhalation to
expel CO2 and recruit 02
- Use of accessory muscles to increase chest expansion and help with forced exhalation to
Effects of hypoxaemia?
- Tachypnoea once PO2 < 60mmHg to recruit more 02
- Activation of sympathetic nervous system response (increase Heart rate, Blood pressure)
to increase 02 circulation to tissues - Peripheral vasoconstriction (poor peripheral perfusion) to prevent O2 for vital organs
- Activation of sympathetic nervous system response (increase Heart rate, Blood pressure)
What is the aim of oxygen therapy?
The reversal of Hypoxaemia and Hypoxia
How would you administer oxygen therapy?
- NASAL PRONGS:
- Used when low to medium concentration of 02 is required
- Greater than 4L/min may dry out nasal mucosa
- Useful when the patient is eating and cannot use a face mask
- SIMPLE FACE MASK (may also be called a Hudson Mask):
- Inspired oxygen concentration varies with litre flow, rate and depth of reparations
- There are other types of masks I.e. patient disease-specific
How would you evaluate whether oxygen therapy has been effective?
- Decreased respiratory rate
- Increase in depth of respirations
- Increase tissue oxygenation (mucous membranes, not just Sp02)
- Decrease work of breathing/accessory muscle use
- Decrease work of myocardium in patients with cardiac disease
- Increased Sp02 levels
Why do people with chronic kidney disease have anaemia?
When your kidneys are damaged, they produce less erythropoietin (EPO), a hormone that signals your bone marrow—the spongy tissue inside most of your bones—to make red blood cells. With less EPO, your body makes fewer red blood cells, and less oxygen is delivered to your organs and tissues
How does Heart failure and the Renal System relate to each other?
- Prior heart attack, high blood pressure and coronary artery disease can lead to heart failure and impacts the ability to efficiently pump blood to the rest of the body
- As a result, the heart may beat faster and the left ventricle may increase in size becoming an even less effective pump
- When the kidneys sense the reduced blood flow, they attempt to compensate by retaining more water and salt
- This excess fluid retention often causes congestion in tissues and results in swelling and an increased strain on the weakened heart
- The progressive effect of the heart failing to properly circulate blood and congestion due to fluid retention is known as congestive heart failure
What is the development of peripheral oedema in patients with heart failure from?
Related to fluid excess. As the heart starts to fail, renal perfusion falls. The kidneys respond byincreasing the production of renin, leading to more aldosterone production, which is consequently followed by sodium and water retention with less urine production with these products and try and maintain/increase BP
What are the 2 structures that filter blood for each nephron in the kidney?
- Blob-like structure called Glomerulus
- Long Stringy structure called Tubule
What structure sifts through blood in the kidney?
Nephrons
What do the Glomerulus and Tubule do in the kidneys?
- The glomerulus works like a sift to only allow specific ingredients such as vitamins and minerals to pass into the tubule
- The tubule detects whether any of those ingredients are needed in the body, if they are needed, they are reabsorbed in amounts the body needs so they can circulate in the blood again. The tubules also sense compounds that the body doesn’t need (urea, left over from the breakdown of proteins) and redirect them as urine, transporting it out of the kidneys via 2 ureters
The nurse measures the blood pressure of a 78-year-old patient and finds it to be 168/86 mmHg. An age-related change that contributes to this finding is:
A. Stenosis of the heart valves
B. Loss of elasticity in arterial vessels
C. Decreased beta-adrenergic sensitivity
D. An increase in serum calcium levels
Loss of elasticity in arterial vessels
During an assessment of a 63-year-old at the clinic, the patient tells the nurse that for years they have taken an evening walk, but lately even a short walk causes leg pain and muscle cramps. If they stop for a while, the pain goes away. The nurse recognises this condition as:
A. An arterial inflammatory and spastic condition that is precipitated by exercise
B. Varicose veins due to chronic venous insufficiency, with resultant ischaemia and pain
C. Thrombophlebitis due to a blood clot in a peripheral vessel, resulting in venous obstruction
D. Intermittent claudication due to peripheral ischaemia
D. Intermittent claudication due to peripheral ischaemia
You are talking to your patient several days following their myocardial infarction. During this conversation, you explain that a myocardial infarction is:
A. A blockage of a coronary artery
B. A complication of congestive heart failure
C. Ischemia of the heart muscle
D. A worse form of angina pectoris
A. A blockage of a coronary artery
You are caring for a patient who was admitted with myocardial infarction (MI) two days ago. You note bilateral oedema in your client’s lower extremities. You would plan to do which of the following next?
A. Review the intake and output records for the last two days
B. Change the time of diuretic administration from morning to evening
C. Send a referral to the dietician requesting an increased sodium diet
D. Commence daily weighs
D. Commence daily weighs
The most common complication following myocardial infarction is
A. An arryrhythmia
B. Acute respiratory failure
C. Cardiac arrest
D. Pulmonary embolism
A. An arryrhythmia
Shortly after admission, Mr D becomes cyanosed and agitated. The nurse will:
A. Commence him on oxygen at 8 litres via a mask
B. Undertake an assessment using the rapid assessment framework
C. Give him oxygen at 2 litres via a nasal cannula
D. Get him to take deep breaths to increase his oxygen intake
B. Undertake an assessment using the rapid assessment framework
A patient with acute diarrhoea of 24 hours duration calls the clinic to ask for directions for care. In talking with the patient, the nurse should:
A. ask the patient to describe the character of the stools and any associated symptoms
B. advise the patient to use over-the-counter loperamide to slow gastrointestinal motility
C. inform the patient that laboratory testing of blood and stool specimens will be necessary
D. advise the patient to drink clear liquid fluids with electrolytes
A. ask the patient to describe the character of the stools and any associated symptoms
The information that is most important for the nurse to obtain during the initial assessment of a patient admitted to the ward with vomiting of bright red blood is:
A. current medical problems
B. medications the patient is taking
C. history of prior bleeding episodes
D. vital signs and the early warning score
D. vital signs and the early warning score
Two days following a hemicolectomy the patient complains of gas and abdominal distension. The nurse plans care for the patient, based on the knowledge that the patient’s symptoms occur as a result of:
A. impaired peristalsis
B. irritation of the bowel
C. nasogastric suctioning
D. inflammation of the bowel at the anastomosis site
A. impaired peristalsis
Which of the following early signs could alert you to the presence of hypoxia?
A. Restlessness
B. Cyanosis
C. Lethargy
D. Coma
A. Restlessness
Which of the following terms refers to purulent fluid in the pleuritic cavity?
A. Pleural effusion
B. Pneumothorax
C. Empyema
D. Haemothorax
C. Empyema
A patient is treated in the emergency department for shock following a motor vehicle accident. The nurse knows that shock is a clinical syndrome in which cellular dysfunction and organ failure occur primarily as a result of:
A. Hypertension
B. Loss of blood
C. Severe infection
D. Impaired tissue perfusion
D. Impaired tissue perfusion
While monitoring a patient’s cardiac activity, the nurse recognises that a normal physiological mechanism responsible for an increase in heart rate and force of cardiac contractions is stimulation of:
A. The vagus nerve
B. Chemoreceptors in the vena cava
C. Alpha-adrenergic receptors in the vascular system
D. Baroreceptors in the aortic arch and carotid body
D. Baroreceptors in the aortic arch and carotid body
A patient with hypovolaemic shock has a urinary output of 25 mL/hour. The nurse understands that the compensatory physiological mechanism involved is:
A. Release of aldosterone, which increases serum osmolarity, causing release of antidiuretic hormone (ADH)
B. Movement of interstitial fluid to the intravascular space, increasing renal blood flow
C. Activation of the sympathetic nervous system, causing vasodilation of the renal arteries
D. Beta-adrenergic receptor stimulation that causes increased cardiac output as a result of increased heart rate and myocardial contractility
A. Release of aldosterone, which increases serum osmolarity, causing release of antidiuretic hormone (ADH)
A patient has been admitted in acute respiratory distress after collapsing while playing netball. Following your assessment, you identify they have ineffective airway clearance and suspect she has pneumonia. You base this on the finding of
A. oxygen saturations of 85%.
B. respiratory rate of 28 breaths per minute.
C. crackles in the right and left lobes with pink frothy sputum.
D. crackles in the right and left lobes with productive green sputum.
D. crackles in the right and left lobes with productive green sputum.
Your patient is commenced on oxygen therapy. A priority assessment of Mrs White while she is on oxygen will be her
A. respiratory rate
B. accessory muscle use
C. urinary output.
D. oxygen saturation.
A. respiratory rate
The primary goal of withholding food and fluids before surgery is to prevent
A. aspiration.
B. distension.
C. infection.
D. obstruction.
A. aspiration.
You are the student nurse caring for a patient with intravenous therapy. You notice that the intravenous cannula insertion site appears swollen and is tender to touch. What is your first action?
A. Stop the infusion and seek assistance immediately.
B. Remove the intravenous fluids from the patient.
C. Flush the luer with 0.9% Normal Saline.
D. Decrease the drip rate so the IV fluids infuse at a slower rate.
A. Stop the infusion and seek assistance immediately.
