Semester One - Perfusion Flashcards

1
Q

Hypertension (what is it, risk factors, treatments, assessments, considerations)

A
  • What is it: Consistently high blood pressure, more than 140/90
  • Risk factors: history, nutrition, obesity, stress, chronic pain, high alcohol intake, drugs, bad stuff.
  • Treatment: ACE inhibtors, calcium channel blockers, diuretics, ARB, lifestyle
  • Assessment: blood tests, urinalysis.
  • Considerations: Lifestyle
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2
Q

Hyperlipidaemia (what is it, symptoms, risk factors, treatment, considerations, assessment)

A
  • What is it: elevation of one or more of lipo protients in blood (bad fats)
  • Symptoms: can lead to atherosclerosis, high blood pressure, cold extremities
  • Risk factors: history, nutrition, obesity, stress
  • Treatment: lifestyle changes – diet. Statins – (statins slow down natural cholesterol production.)
  • Considerations: can show no symptoms but can suddenly rupture causing a stroke or MI.
  • Assessment: blood test, symptoms
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3
Q

Acute coronary syndrome

A

This is most commonly due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque.

  • Ranges in severity from unstable angina (reversible, angina that occurs at rest) to myocardial infarction (heart attack)
  • Heart attack is an extended interruption of blood flow to the heart causing death or damage of heart cells.
    Assessment: ECG
    Treatment: O2 therapy, morphine, asprin
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4
Q

Angina (what is it, symptoms, triggers, treatment)

A
  • What is it: chest pain due to not enough blood flow to the heart.
  • Symptoms: shortness of breath, chest pain, nausea, belching, dull, heavy, crushing. Pain in left arm.
  • Triggers: occur when increased oxygen demand – during exercise, stress.
  • Treatment: GTN spray (acts on vascular smooth muscles to produce arterial and venous vasodilation)
    relieved by rest.
  • Angina is basically a symptom of acute coronary syndrome.
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5
Q

Heart failure (what is it, causes, symptoms, treatment, left side vs right side, considerations)

A
  • What is it: when the heart is unable to meet the body’s needs.
  • Causes: alterations to normal heart function – increased need eg. Pregnancy
  • Symptoms: SOB, low extremity oedema, breathless when lying down, nausea.
  • Treatment: diuretics, ARB or ACE inhibitors then beta blockers, improving signs and symptoms, decrease hospital admission, goals.
  • Left side heart failure: this is the cause of right sided heart failure, respiratory symptoms due to backflow of blood in to lungs.
  • Right sided heart failure: impacts body. Engorgement of abdominal organs.
  • Considerations: imbalance of fluids, acid/base, imbalance due to medication, imbalance in RAAS.
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6
Q

What is COPD?

A

COPD – umbrella term for chronic bronchitis, asthma and emphysema

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7
Q

Chronic bronchitis (what is it, causes, symptoms, treatment, assessment, considerations)

A
  • What is it: Inflammatory process causing injury which causes changes in bronchi and bronchioles.
    It is a chronic inflammation that destructs celia, thickens the bronchial cell wall creating a thick mucus impacting normal respiration.
  • Causes: smoking, pollution
  • Symptoms: hypoventilation (lack of gas exchange) and hypercapnia (too much O2), cough, struggling to breathe on exertion, cyanosis, breathing out issues.
  • Treatment: do not use oxygen therapy as it can make the hypoxic drive think that it doesn’t need to breathe anymore, bronchodilators.
  • Assessment: pulmonary function test, blood gas.
  • Considerations: quit smoking, smelly jobs – paint etc. avoid infection, preventing further infection.
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8
Q

What is the hypoxic drive?

A

The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.

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9
Q

Emphysema (what is it, causes, symptoms, treatment, assessment)

A
  • What is it: permanent damage to alveoli making the lungs less able to recoil. Meaning old air gets trapped in the lungs which means good oxygen rich air cannot fit.
  • Causes: smoking
  • Symptoms: lack of gas exchange, laboured breathing, pigeon chest, air trapping.
  • Treatment: no treatment
  • Assessment: blood gas
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10
Q

Chronic asthma (what, causes, symptoms, treatment, assessment)

A
  • What is it: inflammation of the bronchioles due to hyper responsiveness of the airways. Airways respond in an abnormal exaggerated response. Inflammatory mediators released – histamine, mast cells and prostaglandins causing oedema restricting airways.
  • Causes: dust, cockroaches, exercise, allergies.
  • Symptoms: wheeze, SOB, bronchospasm, swelling, mucous plug formation.
  • Treatment: managing symptoms, avoiding triggers, inhalers.
  • Assessment: peak flow, skin allergies, triggers, signs and symptoms, use of accessory muscles, LLFRP (look, listen, feel, rate, position)
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11
Q

Tuberculosis (what, considerations, symptoms, assessment)

A
  • What is it: bacteria enters respiratory tract via airbourne droplets –> activate immune response. Macrophages catch them and isolate them – this will be latent as the person is asymptimatic. This can change if the person has low immunity and TB symptoms can arise. In other cases TB can overwhelm the immune system and person becomes symptomatic and very sick.
  • Considerations: can be asymptomatic.
  • Symptoms: fever, night sweats, cough, weight loss.
  • Assessment: sputum sample.
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12
Q

Rheumatic fever and pharyngitis (what, causes, treatment, symptoms)

A
  • What is it: Develops following a pharyngitis infection, Group A Beta hemolytic streptococcus (GAS) attaches to epithelial cells of upper respiratory tract, produces a series of enzymes that invade and damage human tissue.
    Causes: pharyngitis - direct contact with secretions.
    Treatment: pharyngitis - antibiotics
    Symptoms: pharyngitis (sore throat), generalized inflammatory response – pain in joints, limited range of motion due to inflammation, polyarthritis is usually earliest and most frequent sign.
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13
Q

What sort of risk factors may the nurse notice at a pre op assessment that might impact on their anesthetic risk and post op recovery?

A
Medical History
Medication use
Physical limitations/Disabilities
Surgical/Anaesthetic History
Psychosocial/Emotional status
Baseline observations i.e. weight, vital signs
Consent and pt. understanding/education
Post op support
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14
Q

There are two principal components to the stress response to surgery:

A

the neuroendocrineresponse and thecytokineresponse.

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15
Q

What can stimulate the neuroendocrine and cytokine response following surgery?

A
  • noxious afferent stimuli
  • local inflammatory tissue factors
  • pain and anxiety
  • starvation
  • hypothermia and shivering
  • haemorrhage
  • acidosis
  • hypoxemia
  • infection
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16
Q

How can the cytokine response be minimised?

A

It is diminished by minimally invasive surgery, especially laparoscopic techniques. This is because the cytokine component of the stress response is stimulated bylocal tissue damageat the site of the surgery itself and is not inhibited by regional anesthesia.

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17
Q

What stimulates the neuroendocrine response?

A

The neuroendocrine response is stimulated by painful afferent neural stimuli reaching the CNS. It may be diminished and sometimes eliminated altogether by dense neural blockade from a regional anesthetic technique.

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18
Q

What are cardiovascular complications that can occur post-operatively?

A
Haemorrhage
Hypotension and Shock
Arrhythmias
MI
Hypertension
CVA
Deep vein thrombosis
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19
Q

What are some respiratory complications that can occur post-operatively?

A
Atelectasis/Pneumonia
Hypoventilation
Airway obstruction
Pulmonary oedema
Pulmonary Embolism
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20
Q

What are some renal complications that can occur post-operatively?

A

Urinary Retention

Acute Kidney Injury

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21
Q

What are some GI complications that can occur post-operatively?

A

Post op ileus (paralytic ileus)
Acute gastric dilation
Post op nausea and vomiting
Constipation

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22
Q

What are some cognitive complications that can occur post-operatively?

A
Delirium
Hypoxia
Perioperative stroke
Medications effects
Electrolyte abnormalities
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23
Q

Angiotensin Converting Enzyme (ACE) Inhibitor (how do they work, side effects, uses and common suffix)

A
How do they work? 
 Angiotensin 2 increases BP. 
- ACE inhibitors bind to ACE in the RAAS system to prevent the production of angiotensin 2, reducing vasoconstriction.
- Prevents release of aldosterone
What are some common side effects?
-	Dizziness
-	Headache 
-	Low BP
-	Dry cough 
-	Rash
Example: Used to lower BP, (usually ends in ‘pril’).
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24
Q

Calcium channel blockers (how do they work, side effects, uses and common suffix)

A

How do they work?

  • Inhibit the movement of calcium ions across cell membranes of myocardium and arterial muscle cells
  • This alters action potential and blocks muscle cell contraction
  • Depresses myocardial contractility
  • Relaxes and dilates arteries
  • Decreases BP and venous return
What are common side effects? 
-	Light headedness
-	Dizziness
-	Low BP
-	Constipation 
-	GI upset
-	Peripheral oedema – not pushing the blood/fluid around.
Examples: used for hypertension (sometimes ends in ‘dine’)
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25
Q

Angiotensin 2 receptor blockers (ARB) (how, side effects, examples and suffix)

A
How do they work? 
-	Works on RAAS system 
-	Block the action of angiotensin 2 by preventing angiotensin 2 from binding to angiotensin 2 receptors on the muscles surrounding blood vessels. As a result, blood vessels dilate and blood pressure is reduced. Stopping aldosterone (the end product)
What are common side effects? 
-	Low BP 
-	Headache 
-	Fainting 
-	Dizziness
-	GI upset 
-	Back pain
Examples: Used to lower BP. (Ends in ‘tan’.)
26
Q

Diuretics (how, side effects, examples, suffix)

A
How do they work? 
-	Works on kidney nephrons
-	Help get rid of sodium and water in urine resulting in decrease in plasma volume which results in a decrease in BP.
What are common side effects? 
-	Hyponatraemia (low sodium) 
-	Headache
-	Dizziness
-	Thirst 
-	Frequent urination 
Examples: used in hypertension (ends in ‘zide or ide’)
27
Q

Lisinopril, Captopril, Enalapril, Quinapril, Ramapril. What kind of medications are these?

A

Angiotensin converting enzyme (ACE) inhibitors

28
Q

Immediate release – felodipine, amlodipine
Sustained release/extended release/controlled release – diltiazem, Nifedepine, verapamil. What kind of medication are these?

A

Calcium channel blockers

29
Q

Thiazide, bendrofluazide, chlorothiazide, hydrochlorothiazide, frusemide, bumetanide, amiloride acetazolamide, brinzolamide. What kind of medication are these?

A

Diuretics

30
Q

Losartan, Candesartan, Irbersartan what kind of medications are these?

A

Angiotensin receptor blocker (ARB)

31
Q

What is the standard fluid formula for paediatrics?

A
  • Up to 10 kg
    100 mL / kg/ 24 hours
  • 11 to 20 kg
    1000 mL + 50 mL / kg / 24 hours
  • Greater than 20 kg
    1500 mL + 20 mL / kg / 24 hours
32
Q

How is medication in children different from adults?

A
  • water content decreases with age
  • less body fat
  • age effects how drugs are processed
  • erratic blood flow
  • vulnerable to toxicity
33
Q

How do children differ from adults? (there’s heaps, just name a few)

A
  • Immature temperature regulation
  • Immature immune system
  • Less overall organ maturity
  • Greater surface area to body mass ratio
  • Healthier circulatory systems
  • Less muscle mass
  • Increased metabolic rate: increased oxygen demand
  • Great ability to compensate
  • Lower blood pressure ranges, higher HR & RR
  • Brain tissue is softer, thinner, more flexible = greater potential for injury
  • Smaller airway
  • Infants obligatory nose breathers
  • Using accessory muscles may be normal
  • Increased cardiac output/maintained by increased heart rate
  • Children are heart rate dependent: single most important V.S. in assessing perfusion, shock
  • Hypotension a late sign
  • Tachycardia: early sign of distress
  • Bradycardia: indicator of hypoxia
34
Q

Why might you use oxygen therapy?

A
  • Myocardial infarction but only if associated with hypoxemia (
35
Q

What are some symptoms of hypoxia?

A
  • Agitation
  • Labile emotions/personality change
  • Headache
  • Nausea
  • Poor memory
  • Tachycardia
  • Sob
  • Cyanosis
36
Q

Why assess arterial blood gasses?

A
  • Arterial blood gases are needed to obtain evidence of hypoventilation (raised PaCO2) as a reason for hypoxaemia
  • Arterial blood gases may also give an indication of the metabolic effects of clinically important hypoxaemia and respiratory/metabolic acidosis
  • PaCO2 measures the amount of carbon dioxide dissolved in plasma- partial pressure/tension
  • PaO2 measures the amount of oxygen dissolved in plasma- partial pressure/tension
37
Q

What is the difference between hypoxia and hypoxaemia?

A

Hypoxemia (low oxygen in your blood) can cause hypoxia (low oxygen in your tissues) when your blood doesn’t carry enough oxygen to your tissues to meet your body’s needs.

38
Q

What are the different types of oxygen therapy?

A
  • High concentration oxygen therapy:
    Adequate to meet all inspiratory requirements – not dependant on patient’s inspiratory effort
    Provides complete inspiratory volume- high flow devices deliver it’s O2 very accurately
    High flow systems can delivery both high and low concentrations of O2
    Device: venturi mask
  • Low concentration oxygen therapy:
    Used to correct hypoxaemia by using an accurate amount of oxygen, without depleting existing maintenance of carbon dioxide and respiratory acidosis. Blood gases should be used to measure the precise concentration of oxygen
    O2 is delivered to supplement the patient’s tidal volume – oxygen deliver is dependant on patient’s respiritory effort
    Devices include: nasal cannula, Hudson mask, reservoir or non-rebreather masks
  • Long term oxygen therapy (LTOT):
    For patients with chronic hypoxaemia
    Requirements vary between 24-hour dependency and dependency during periods of sleep.
    Principally aims to improve symptoms and prevent harm from chronic hypoxaemia
    Based on an arterial blood gasses and then guided by oximetry
    Treatment goal is to match supplementary oxygen to oxygen requirements - usually above 89%
39
Q

budesonide, fluticasone, beclomethasone, what kind of medications are these?

A

Glucocorticosteroids.

40
Q

Glucocorticosteroids (how does it work, side effects)

A
  • Work by reducing inflammation – inhibits mast cell rupture, decreases the synthesis of inflammatory mediators, stops new antibody production, suppresses activity of immune cells (lymphocytes & macrophages)
  • Works slowly over a period of hours and may take 6 to 12 weeks to reduce airway inflammation
  • side effects: Oral Candida, hoarse voice
    Prolonged use at high doses or frequent oral administration – thin skin that bruises easily , weight gain, drug induced Cushing’s syndrome, temporary growth disturbance in children, reduced bone mineral density -osteopenia, osteoporosis, type 2 diabetes
41
Q

Short-acting: ipratropium bromide, oxytropium bromide
Long-acting: tiotropium bromide (fully subsidised under Special Authority)
What are these medications?

A

Anticholinergics

42
Q

Anticholinergics/muscarinics (how do they work, side effects)

A
  • Blocks muscarinic /cholinergic receptors associated with parasympathetic stimulation of bronchial smooth muscle causing bronchodilation via relaxation of smooth muscle
  • Causes reduction of the viscous mucus secretion associated with COPD
  • Much slower onset that beta 2 agonists
    Side effects: dry mouth, pupil dilation, glaucoma, urinary retention = decreased voiding leads to retention of urine (particularly elderly men)
  • Can be combined with a beta 2 agonist - Combivent -Salbutamol and Atrovent
43
Q

Is it better to have a smaller cannula in a patient? Why/why not?

A

The smaller the better

  • greater blood flow and haemodilution reducing damage to intima from irritant solutions
  • reduced mechanical irritation and insertion trauma
44
Q

What are some on-going cares required for a cannula?

A

What - Access bung after swabbing, using aseptic non-touch technique

  • Flush with 0.9% sodium chloride to review patency each shift unless in more frequent use
  • Use turbulent flushing to wash the line
  • Use SAS technique – syringe directed to device
  • Use positive pressure technique for locking
  • A sterile, semi-permeable, transparent dressing must remain dry and intact or is changed immediately
  • If the insertion site is obscured by an opaque dressing, preventing visual inspection, this dressing must be changed
  • PIVC insertion sites must be revealed and inspected each shift, (daily in the community) and every time the cannula is accessed, or infusion rates are altered
45
Q

What is phlebitis? How is it scored?

A

Inflammation of the walls of the vein. It is scored 0-5. 0 is no signs of phlebitis, 5 is advanced stage.

46
Q

What is the SAS protocol?

A

S - saline flush
A - administer medication
S - saline flush

47
Q

What does “no dwell time” mean in relation to I.V therapy?

A

It means to take the cannula out when it is no longer required.

48
Q

What does the chain of survival consist of?

A
  • prevention
  • early recognition
  • early activation of emergency medical systems
  • early CPR
  • early defibrillation
  • early advanced care

This will give the patient the best chance of survival - a break in the chain will decrease survival rate

49
Q

What is an arrest caused by in an adult and in a child?

A

Adult - cardiac arrest caused by cardiac arrhythmia
Child - primary cause of a arrest usually from respiratory failure (obstruction, SIDS, drowning, sepsis, poisoning, neurological disease)

50
Q

What does DRSABCD stand for?

A
Danger 
Responsiveness
Send for help 
Airway 
Breathing
Circulation 
Defibrillation
51
Q

How would you know if an adult had a complete or partial airway obstruction?

A

Partial - distressed and coughing
Complete - stridor, cyanosis, no air is being moved. Commence 5 back blows, 5 chest thrusts continue until relieved or when person becomes unresponsive.

52
Q

What are the four primary characteristics of the cells that sit in the heart?

A
  1. Automaticity - generation of spontaneous impulses
  2. Excitability - respond to electrical impulses
  3. Conductivity - conduct electrical impulses
  4. Contractility - ability to cause muscle contraction
53
Q

What are the three main functions of the AV node?

A
  1. Slow electrical impulse through AV node (PR interval)
  2. Back up pacemaker
  3. Block some impulses to avoid dangerously rapid rates
54
Q

What is sinus tachycardia?

A
  • A normal response to an increased demand in blood flow (eg. during exercise)
  • Can be caused by pain, fever
  • Begins and ends gradually
55
Q

What is sinus bradycardia?

A
  • normal response to relaxation

- parasympathetic system takes over

56
Q

What is dyspnoea?

A

Dyspnoea, also known as shortness of breath or breathlessness, is a subjective sensation of breathing discomfort.

57
Q

What is atrial fibrillation?

A
  • This is when the electrical impulses from the atria controlling the rate and rhythm get disorganised.
  • This causes the atria to quiver resulting in increased myocardial oxygen demand and increased cardiac output.
58
Q

What is ventricular fibrillation?

A

Abnormal electrical impulses are produced in the lower chambers of the heart causing the heart to pump faster. This means that the ventricles do not have enough time to fill up with blood properly - not enough blood being pumped around the body.
This is the most common cause of cardiac death.

59
Q

What is a cardiac arrest?

A

During an arrhythmia, the heart can beat too fast, too slow, or it can stop beating. Cardiac arrest occurs when the heart develops an arrhythmia that causes it to stop beating.
(This is different than a heart attack, where the heart usually continues to beat but blood flow to the heart is blocked.)

60
Q

How does the RAAS system work?

A
  • In response to low blood pressure, the liver releases angiotensinogen.
  • In response to this, kidney releases renin
  • They react and make angiotensin 1
  • When angiotensin 1 gets to lungs, it releases ACE which makes angiotensin 2.
  • Angiotensin 2 then goes adrenal gland and becomes aldosterone.