Guided Studies Flashcards
(142 cards)
1
Q
Identify some general principles of presrcibing on the hospital drug kardex.
A
- All patients should have one (even if not currently on any medication, should still contain any drug allergies)
- All drugs to be administered should be prescribed, including oxygen and complementary medicines. (if emergency, can prescribe after use it)
- Only registered medical, dental and non-medical prescribers can prescribe “prescribe-only” drugs
- In English, not latin
- In BLOCK CAPITALS
- General drug name rather than brand name (unless insulin, combination drugs)
- 24 hour clock used for time of administration
- Start date and signature required
- Once patient leaves, kardex put on patient records
2
Q
Why is it important than the signature of the prescriber is included ?
A
So potential queries can be directed to the right person
3
Q
Identify acceptable abbreviations to be used for routes of admin in a drug kardex.
A
Intravenous = IV Sublingual = SL Nasogastric = NG Per vagina = PV Per rectum = PR Topical = TOP Intramuscular = IM Subcutaneous = SC Inhalation = INH Oral NOT shortened (could be interpreted as a zero)
4
Q
Identify acceptable abbreviations to be used for doses in a drug kardex.
A
mg
g
Micro grams and Nano grams spelled out
Units spelled out
5
Q
.5 or 0.5 ?
A
0.5
6
Q
1,000 or 1000 ? Why ?
A
1000 because , can be confused with decimal point
7
Q
500 mg or 0.5 g ?
100micrograms or 0.1 mg ?
0.1 microgram or 100 nanograms ?
A
500 mg because quantities less than 1 g should be written in mg
100 micrograms because quantities less than 1 mg should be written in microgram
100 nanograms because quantities less than 1 microgram should be written in nanograms
8
Q
Give examples of controlled drugs. How is prescription on kardex performed for these drugs ?
A
Oxycodone, morphine, Temazepam
CDs are prescribed on the hospital kardex the same way as other drugs. Stored in a specific locked cupboard on the ward, and a register is held and updated whenever a CD is taken out of the cupboard, signed by 2 health professionals before administration to the patient.
On the discharge prescription (or GP prescription) a pharmacist is not allowed to dispense a CD unless all the information required by law is given on the prescription.
9
Q
What information must be on hospital discharge or GP prescriptions
involving controlled drugs ?
A
- Name + address of patient
- Name + form + dose + administration + strength of drug
- Total quantity supplied in letters and numbers
- Signature and date by prescriber
10
Q
What does NKDA stand for ?
A
No known drug allergies
11
Q
If the patient has no allergy should you leave the allergies box blank ?
A
No, write NKDA
12
Q
Define “non-administration codes”.
A
Abbreviations used when the prescribed drug was not able to be given (e.g. patient refused, patient unavailable, nausea and vomiting)
13
Q
Which type of drugs are once only prescriptions usually for ?
A
Analgesics, pre or post-operative drugs,
and single doses of antibiotics
14
Q
What is another name for prescription only medicines ?
A
Stat doses
15
Q
What type of drugs are as required prescriptions for ?
A
Analgesics, laxatives and antiemetics (max dose must be specified)
16
Q
How is warfarin prescribed on the cardex ?
A
Should be in the anticoagulant/warfarin chart + in the main kardex (administration times etc. should be done on the anticoagulant/warfarin chart)
17
Q
Identify the main features of transverse sections of cardiac muscle.
A
- dotted appearance of fibres. Each ‘dot’ is a myofibril
- fibres are narrower than those of striated voluntary muscle
- the nuclei lie in a central position, but the plane of the section does not always pass through the nucleus
- delicate connective tissue (endomysium) supports the rich capillary bed surrounding the muscle fibres
18
Q
Identify the main features of longitudinal sections of cardiac muscle.
A
- there is extensive branching of the muscle fibres (not seen in striated voluntary
muscle, except in the tongue) - faint cross striations similar to those of striated muscle
- intercalated discs which are thin lines passing at intervals across the thickness of the muscle fibres – some straight and some in step-wise manner. These discs are unique
to cardiac muscle - endomysium and blood capillaries in the slit-like spaces between the fibres
- the nuclei are oval
19
Q
Identify the main features of transverse sections of smooth muscle.
A
-Individual cells vary in diameter depending on their location within the cell. Cross-sections through the middle of cells have centrally located nuclei, usually surrounded by an unstained region.
20
Q
Identify the main features of longitudinal sections of smooth muscle.
A
- Relaxed: the nuclei are elongated with rounded ends.
- Contracted: the nuclei spiral, kink, or twist. The cytoplasm is pink, non-striated and with little detail.
21
Q
Identify the main features of transverse sections of skeletal muscle.
A
Polygonal cross-sections (50 to 150 µm in diameter) with nuclei at the periphery.
22
Q
Identify the main features of longitudinal sections of skeletal muscle.
A
Cells can vary in length from a few millimeters to almost a meter.
-Myofibrils: the cytoplasm is filled with myofibrils that extend the entire length of the cell. Individual myofibrils are only seen where they are slightly separated.
-Sarcomeres: myofibrils show an alternating series of striations due to the repeating sarcomeres.
A band - the main dark band
I band - the main light band
H band - thin light band in the middle of the A band
Z band - thin dark line in the middle of the I band
23
Q
Complete the following for cardiac muscle:
- Location(s) in the body
- Cell shape and appearance
- Connective tissue components
- Are there myofibrils and are they arranged in sarcomeres?
- Are there T-tubules? Where are they?
- Is there an elaborate SR?
- Are there gap junctions between the cells?
- Do the cells exhibit individual neuromuscular junctions?
- How is contraction regulated?
- What is the source of the Ca2+ for contraction?
- What does Ca2+ interact with?
- Is there a pacemaker?
- How fast is contraction?
- What is the muscle’s response to stretch?
- Is the muscle respiring aerobically or anaerobically or both?
A
- Location(s) in the body: “muscular wall of the heart (i.e. myocardium). Some cardiac muscle is also present in the walls of the aorta, pulmonary vein, and superior vena cava”
- Connective tissue components: “epimysium, the sheath of connective tissue that surrounds muscles; perimysium, which is associated with groups of cells; and endomysium, which surrounds and interconnects individual muscle cells.”
- Are there myofibrils and are they arranged in sarcomeres? Yes and yes
-Are there T-tubules? Where are they?
Yes, run from the surface to the cell’s interior (“invaginations of external membrane of muscle cells”)
- Is there an elaborate SR? Yes
- Are there gap junctions between the cells? Yes (as part of intercalated discs)
- Do the cells exhibit individual neuromuscular junctions? No
- How is contraction regulated? By intracellular Calcium
- What is the source of the Ca2+ for contraction? Mainly Calcium from SR (but also some from extracellular)
- What does Ca2+ interact with? Extracellular calcium enters cell through DHPR, in T-tubule membrane, binds RYR, opens it, and causes release of more calcium.
- Is there a pacemaker? Yes
- How fast is contraction? Quick contractions
-What is the muscle’s response to stretch?
Increased contraction
-Is the muscle respiring aerobically or anaerobically or both? Mainly aerobically (can be anaerobic during “ brief periods of oxygen deprivation”)
24
Q
Describe the microscopic appearance of cardiac muscle. Draw it.
A
Braching and anastomosing shorter fibers with transverse striations running parallel and connected end to end by complex junctions (intercalated discs). Single, centrally located nucleus.
Refer to “Clinically Oriented Anatomy”
25
Describe the microscopic appearance of smooth muscle. Draw it.
Single, or agglomerated. Small, spindle-shaped fibers without striations. Single central nucleus.
Refer to "Clinically Oriented Anatomy"
26
Describe the microscopic appearance of skeletal muscle. Draw it.
Large, very long unbranched cylindrical fibers with transverse striations arranged in parallel bundles. Multiple, peripherally located nuclei.
Refer to "Clinically Oriented Anatomy"
27
List the three major types of blood vessels .
Arteries
Veins
Capillaries
28
Describe (with the aid of a diagram) the basic composition of the wall of a blood
vessel.
-Tunica intima: contains endothelium (continuation of the endocardial lining of the heart) which forms a slick surface that minimizes friction as blood moves through the lumen. In vessels larger than 1 mm in diameter, a subendothelial layer of loose connective tissue (a basement membrane) supports the endothelium.
-Tunica media: mostly circularly arranged smooth muscle cells (where vasodilation and contraction can occur) and sheets of elastin.
Generally, the tunica media is the bulkiest layer in arteries.
-Tunica externa/adventitia: composed largely of loosely woven collagen fibers that protect and reinforce the vessel, and anchor it to surrounding structures. Infiltrated with nerve fibers, lymphatic vessels, and, in larger veins, a network of elastin fibers. In larger vessels, the tunica externa contains the vasa vasorum (nourish the more external tissues of the blood vessel wall). The innermost or luminal portion of the vessel obtains its nutrients directly from blood in the lumen.
29
Given that the more external tissues of blood vessel walls are nourished by vasa vasorum contained in the tunica externa, where do the innermost/luminal parts get their blood supply from ?
Directly from the lumen
30
Describe (with the aid of a diagram) the wall of an elastic (=conducting) artery, linking its structure with its function.
- Thick-walled arteries near the heart (e.g. aorta and its major branches)
- Largest in diameter, ranging from 2.5 cm to 1 cm, and the most elastic
- They contain more elastin than any other vessel type. It is present in all three tunics, but the tunica media contains the most. There the elastin constructs concentric "holey" laminae (sheets) of elastic connective tissue that look like slices of Swiss cheese interspersed between the layers of smooth muscle cells. The abundant elastin enables these arteries to withstand and smooth out large pressure fluctuations by expanding when the heart forces blood into them, and then recoiling to propel blood onward into the circulation when the heart relaxes.
- Elastic arteries also contain substantial amounts of smooth muscle, but they are relatively inactive in vasoconstriction.
- The elastic arteries expand and recoil passively to accommodate changes in blood volume so blood flows continuously rather than starting and stopping with the pulsating rhythm of the heartbeat.
31
What are the implications if elastic/conducting blood vessels become hard and unyielding (e.g. atherosclerosis) ?
Blood flows more intermittently. Also, without the pressure-smoothing effect of the elastic arteries, the walls of arteries throughout the body experience higher pressures. Battered by high pressures, the arteries eventually weaken and may balloon out or even burst.
32
Recognise elastic artery histology slides.
Refer to Google.
33
Describe (with the aid of a diagram) the wall of an muscular (=distributing) artery, linking its structure with its function.
- Deliver blood to specific body organs
- Their internal diameter ranges from that of a little finger (1 cm) to that of a pencil lead (about 0.3 mm).
- Proportionately, they have the thickest media of all vessels. Their tunica media contains relatively more smooth muscle and less elastic tissue than do elastic arteries ( Table 19.1 ); therefore, they are more active in vasoconstriction and less distensible.
- In muscular arteries, however, there is an elastic lamina on each face of the tunica media.
34
Recognise muscular artery histology slides.
Refer to Google.
35
Describe the wall of arterioles, linking its structure with its function.
- Lumen diameter ranging from 0.3 mm down to 10 μm.
- Larger arterioles have all three tunics, but their tunica media is chiefly smooth muscle with a few scattered elastic fibers.
- Smaller arterioles, which lead into the capillary beds, are little more than a single layer of smooth muscle cells spiraling around the endothelial lining.
- Minute-to-minute blood flow into the capillary beds is determined by arteriole diameter, which varies depending whether they constrict (the tissues served are largely bypassed) or dilate (blood flow into the local capillaries increases dramatically).
36
Describe the wall of a venule.
- Lumen diameter ranging from 8 to 100 μm
- The smallest venules, the postcapillary venules, consist entirely of endothelium around which a few pericytes congregate. They are extremely porous (more like capillaries than veins in this way), and fluid and white blood cells move easily from the bloodstream through their walls.
- The larger venules have one or two layers of smooth muscle cells (a scanty tunica media) and thin externa as well.
37
Recognise arteriole and venule histology slides.
Refer to Google.
38
Clinically, what is the significance of the porous nature of venules ?
In inflammation, adhesion of white blood cells to the postcapillary venule endothelium occurs, followed by their migration through the wall into the inflamed tissue.
39
Describe the walls of a vein, linking its function with its structure.
- Veins usually have three distinct tunics, but their walls are always thinner (because the blood pressure in veins is low so no danger of bursting) and their lumens larger than those of corresponding arteries
- Consequently, in the view seen in routine histological preparations, veins are usually collapsed and their lumens appear slitlike.
- There is relatively little smooth muscle or elastin in the tunica media, which is poorly developed and tends to be thin even in the largest veins.
- The tunica externa is the heaviest wall layer. Consisting of thick longitudinal bundles of collagen fibers and elastic networks, it is often several times thicker than the tunica media. In the largest veins--the venae cavae-the tunica externa is further thickened by longitudinal bands of smooth muscle.
- With their large lumens and thin walls, veins can accommodate a fairly large blood volume (i.e. capacitance vessels and blood reservoirs)
- The low-pressure condition demands some adaptations to ensure that blood is returned to the heart at the same rate it was pumped into the circulation. The large-diameter lumens of veins (which offer relatively little resistance to blood flow) are one structural adaptation. Another is valves that prevent blood from flowing backward.
- Venous valves are formed from folds of the tunica interna. Venous valves are most abundant in the veins of the limbs, where the upward flow of blood is opposed by gravity. They are absent in veins of the ventral body cavity.
40
Recognise a vein histology slide.
Refer to Google.
41
Recognise the tunia intima, media and adventita on a histology slide.
Refer to Google.
42
What is so special about the structure of coronary and dural sinuses ?
- Venous sinuses, such as the coronary sinus of the heart and the dural sinuses of the brain, are highly specialized, flattened veins with extremely thin walls composed only of endothelium. They are supported by the tissues that surround them, rather than by any additional tunics.
- The dural sinuses, which receive cerebrospinal fluid and blood draining from the brain, are reinforced by the tough dura mater that covers the brain surface.
43
Identify possible reasons to use a central line.
• Measurement of central venous pressure (CVP)
• Administration of drugs or products that would damage smaller caliber veins such as
chemotherapy or parental nutrition
• Need to obtain venous access in a patient whose peripheral veins are shut down e.g.
a patient with shock
• Administration of high flow fluids
• Ease of administration of products in a patient likely to need intravenous access for
several days e.g. post major abdominal surgery
44
What are the most common sites for central line insertion ?
• Internal jugular vein (usually on the right)
• Subclavian vein (usually on the right)
The femoral vein and external jugular vein can also be used but less commonly
45
Explain the process of inserting a central line.
1) Central lines are placed with the patient lying down and facing away from the site of
insertions to aid identification of the vein.
2) Ultrasound should be used to ensure that the needle is placed correctly and not inserted into the internal carotid or subclavian arteries.
3) After the vein has been correctly located a guide wire is passed through the needle into
the vein. The cannula or catheter is then passed over the guide wire into the vein
The guide wire can then be removed.
46
What is the use of having multi-lumen central lines ?
This allows different fluids and drugs to be given at the same time whilst the CVP is being measured from a different connection.
47
What do a high and a low CVP indicate respectively ?
High CVP- Right Heart Failure
| Low CVP- veinous return to the heart is less than it should be (e.g. due to hypovolaemic shock or dehydration)
48
Identify complications of central line insertion.
- Puncturing the apex of the lung, superior to the clavicle, resulting in a pneumothorax
- Puncturing a major vessel as well as a lung resulting in a haemothorax
- Accidentally cannulating a large artery
- Damage to the thoracic duct (if playing line on the left)
- Introducing air into the circulation while inserting the line and causing an air embolism
- If inserted under un-sterile conditions, risk of infection to a major blood vessel and into the bloodstream (risk even if sterile conditions)
- Risk of damage to anomalous veinous valves which may result in thrombus formation
49
Why are most central lines only inserted for as short a time as possible ?
They are uncomfortable for the patient and there is a higher risk of introducing infection into the bloodstream the longer that they are left in position.
50
What can we use instead of a central line if access is needed for a longer period of time ?
A special kind of cannula can be inserted such as one with a port placed under the skin.
51
Clearly differentiate the terms hypoxia and hypoxaemia.
-Hypoxaemia = low PO2 or partial pressure of oxygen (PaO2) in the blood
-Hypoxia = oxygen supplies are insufficient
to meet oxygen demands in a particular compartment (e.g. alveolar or tissue hypoxia)
52
Which is the most sensitive organ to the effects of hypoxia? How might this present?
Brain.
| Impaired mental functioning even in healthy participants.
53
What are the “five vital signs?”
```
Pulse rate
Blood pressure,
Temperature
Respiratory rate
5th: oxygen saturation by pulse oximetry in all breathless and acutely ill
patients
```
54
It is recommended that oxygen is prescribed to achieve a “target saturation”. What
targets does the Guideline suggest for:
a. most acutely ill patients?
b. those patients at risk of hypercapnic respiratory failure?
- For most acutely ill patients: 94-98%
| - For patients at risk of hypercapnic respiratory failure: 88-92%
55
Which clinical conditions does the Guideline suggest oxygen therapy is indicated
for despite the absence of low oxygen saturation? Explain why.
♦ Carbon monoxide: apparently ‘normal’ oximetry reading may be produced by carboxyhaemoglobin, so aim at an oxygen saturation of 100%
♦ Cyanide poisoning: leads to histotoxic
hypoxia
56
Where should the ball of a flow meter device sit to correctly deliver the required
amount of oxygen?
The centre of the ball should be aligned with the appropriate flow rate marking.
57
In addition to the patient’s identity, date and signature of the clinician what other details should be clearly outlined in all prescriptions for oxygen ?
- Target saturation range rather than prescribing a fixed concentration of oxygen or FiO2
- Oxygen saturation
- Delivery system (including flow rate)
58
Briefly explain the Vincristine Case.
Vincristine wrongly administered intrathecally - into the cerebrospinal fluid.
59
Describe three possible solutions, outlined by Noble and Donaldson, to prevent wrong route delivery medication errors, illustrating your answer with reference to vincristine
"- Drug alerts that warn healthcare institutions, medical practioners and other relevant personnel about new risks
- Development of consensus and evidence-based protocols and guidelines to create a standard operating procedure that prevents against error
- Physical redesign of delivery systems such that it is impossible to deliver drugs by the wrong route
Attempts to create delivery systems whereby IV and intrathecal drug can physically only be given by their designated routes. The use of a mini bag to deliver vincristine has become increasingly discussed and advocated. It involves not using syringes to deliver vincristine at all and instead diluting the drug in a mini bag working in the premises that it would be virtually impossible to deliver this to a patient through a spiral needle." (Quizlet)
60
Describe the five domains of failure, outlined by Noble and Donaldson, which they believe have been present in the area of intrathecal vincristine administration error.
"- failure to learn from adverse events
- failure of international translation
- failure to achieve compliance with safety guidance
- failure of investigations and enquiries
- failure of solutions" (Quizlet)
61
Describe the micro and macroscopic changes up to 18 hours after an MI.
MACRO: None
MICRO: Non
62
Describe the micro and macroscopic changes 24-48 hours after an MI.
MACRO: Pale, oedematous muscle
MICRO: Oedema, neutrophil infiltration, necrosis of myocytes
63
Describe the micro and macroscopic changes 3-4 days after an MI.
MACRO: Yellow, rubbery centre with
haemorrhagic border
MICRO: Obvious necrosis and inflammation: early granulation tissue
64
Describe the micro and macroscopic changes 1-3 weeks after an MI.
MACRO: Infarcted area paler and
thinner than unaffected
ventricle
MICRO: Granulation tissue then progressive fibrosis
65
Describe the micro and macroscopic changes 3-6 weeks after an MI.
MACRO: Silvery scar becoming white and tough
MICRO: Dense fibrosis
66
Define shock.
Insufficient blood supply to the tissues, to meet their demands.
67
What does perfusion to tissues depend on ?
- The pumping ability of the heart to maintain a perfusion pressure
- Sufficient blood to fill the circulation
- A vascular system that moves blood around the body and back to the heart
- Tissues that are able to extract and use nutrients
68
Identify and define the main types of shock.
1) Cardiogenic
2) Hypovolaemic
3) Obstructive
4) Distributive
69
Define cardiogenic shock.
Heart unable to maintain adequate blood supply (decreased CO). Could be due to failure of heart as a pump (myocardial damage), severe alterations in rhythm such that contraction is not coordinated, or a mechanical defect (valve damage allowing blood to flow the wrong way).
- After-load is also increased due to increased systemic resistance + end-systolic ventricular volume (pre-load) is increased.
- Lips, nail beds and skin are cyanosed
- Blood flow can stagnate, causing production of thrombi/emboli.
- Central venous pressure rises as a result of volume overload caused by the pumping failure of the heart
70
Define hypovolaemic shock.
Decrease in circulatory volume. Could be due to diminished blood volume, loss of whole blood, loss of plasma, loss of ECF.
71
Define obstructive shock.
Could be due to inability of the heart to fill adequately, or obstruction to outflow from the heart (aortic aneurism, cardiac tamponade, pneumothorax, pulmonary embolism).
72
Define distributive shock.
- Loss of sympathetic vasomotor tone (i.e. loss of blood vessel tone, due to damage to CVS center in medulla or damage to sympathetic outflow OR due to presence of vasodilatory substances in blood such as histamine)
- Enlargement of the vascular compartment (i.e. volume of blood normal but volume of vascular compartment increased)
- Fluid shifts away from the heart and central circulation e.g. shunting of vascular fluid to interstitial spaces, arterio-veinous shunting
- Can also be associated with failure of the cells to use oxygen (e.g. poisoning).
73
Identify the main forms of distributive shock.
Anaphylactic, septic, neurogenic
74
What is another name for distributive shock
Normovolaemic shock
75
# Define the main features of anaphylactic shock, including:
- Characteristics
- Causes
- Timeline
- Characteristics: Massive vasodilation, pooling of blood in the peripheral vessels and increased capillary permeability. Often accompanied by life-threatening laryngeal oedema. It can also manifest itself as bronchospasm and contraction of GI and uterine smooth muscle.
- Cause: Due to an immunologically mediated reaction in which vasodilators such as histamine are released into the blood.
- Timeline: rapid, death can occur within minutes if untreated.
76
Identify common antigens associated with anaphylactic shock.
Drugs (penicillin), shellfish, nuts, animals, insect stings and tetanus antitoxin
77
What are the signs and symptoms of anaphylactic shock ?
Abdominal cramps, burning skin, itching, coughing, wheezing
Precipitous drop in blood pressure
Pulse may become difficult to detect
78
What is the treatment of anaphylactic shock ?
♦ Prompt discontinuance of agent
♦ Application of measures to reduce
absorption (where applicable – e.g. ice to bee stings)
♦ Monitoring of CV and respiratory
function, maintenance of gas exchange and perfusion.
♦ Adrenaline constricts blood vessels and
relaxes airways.
♦ Antihistamines, corticosteroids and oxygen can also be administered.
79
Describe the main characteristics of septic shock.
- Characteristics:
- Causes
-Causes: Due to a widely disseminated infection (Gram-ve bacteria, fungi, viruses) and the release of inflammatory mediators into the systemic circulation. Commonly associated with other pathologic conditions, and can be due to peritonitis, abortion, rupture of the gut, skin infection,
inflammatory and immune responses accompanied by histamine release, indwelling urinary or intravenous catheter
-Characteristics: can result in the release of histamine, kinins and prostaglandins as well as the immune and inflammatory responses, causing vasodilatation; pyrogenic substances are also released leading to high fever; there might also be activation of coagulation and fibrinolysis. As sepsis continues, the patient develops a greyish tinge due to stasis of blood in capillary vessels, and cyanosis due to a reduced oxygenation of haemoglobin.
80
What are the most susceptible groups to septic shock ?
The elderly or those with extensive trauma, burns, neoplastic disease or diabetes are particularly susceptible.
81
What are the signs and symptoms of septic shock ?
Fever, vasodilatation, warm, flushed skin, mild hyperventilation, changes
in cerebral blood flow, raised white blood cell counts
82
Describe the main features of neurogenic shock.
- Causes:
- Timeline
- Causes: Due to a defect in the vasomotor centre in the brain stem or the sympathetic outflow to the blood vessels. Vasomotor function can be inhibited by brain injury, depressant action of drugs, anaesthesia, hypoxia or hypoglycaemia. Spinal anaesthesia or spinal cord injury above the mid-thoracic region can interrupt the outflow to blood vessels. Many general anaesthetics can cause neurogenic-shock-like reactions, especially during induction by interfering with sympathetic nervous system function
- Timeline: Rare and usually transitory (e.g. fainting due to emotion)
83
What are the signs and symptoms of neurogenic shock ?
Slower heart rate
| Skin warm and dry
84
Identify the stages of shock.
1) Initial Stage - perfusion is decreased but not enough to cause serious effects
2) Compensatory Stage - perfusion is reduced, but mechanisms are able to maintain BP and tissue perfusion sufficiently to prevent cell damage
3) Progressive stage or stage of decompensated shock - BP starts to fall, blood flow to the heart and brain become impaired, capillary permeability is increased, fluid leaves the capillaries, blood flow becomes sluggish and body cells and their enzyme systems are damaged
4) Irreversible shock - even if blood volume is restored and vital signs stabilise, death ensues
85
What is the aim of compensatory mechanisms in shock ? Identify the compensatory mechanisms of hypovolaemic shock.
Maintain BP and CO and restore circulating volume.
1) Sympathetic-mediated responses
- Quick (within seconds) as a result of baroreceptor reflex
- Sympathetic and adrenal medullary activity increase, leading to tachycardia, increased cardiac contractility, and widespread vasoconstriction - both arterioles and veins (but not to brain or heart is P is above 70 mmHg)
- Vasoconstriction → Increased peripheral resistance (constriction of arterioles) and Veinous return (constriction of veins) → Increased SV (Frank Starling) via increased veinous return
Direct sympathetic stimulation of myocardium → Increased SV via increased contractility
Increased HR → Increased CO (and in turn BP)
If shock progresses, further increases in HR, cardiac contractility and vasoconstriction to skin, skeletal muscles, kidneys, GI organs (non-essential)
2) Mechanisms to restore BV
-Absorption of fluid from interstitial spaces (due to drop in hydrostatic P)
-Conservation of salt and water by kidneys (primarily through renin-angiotensin II-aldosterone + via ADH in severe cases of V loss)
-Changes to distribution between extra and intracellular fluid if change in osmolality
Overall effects of BV mechanisms are shifting volume from cells to circulation, preservation of water and salt, and increase blood volume.
86
Is the sympaethic-mediated response to hypovolaemic shock sufficient ?
Sufficient if the trauma is small, but only for a short time.
87
What are the effects of long term continuation of compensatory mechanisms in hypovolaemic shock ?
Due to positive feedback cycle.
1) Flow in microcirculation
- Vascular system fails
- Relaxation of arterioles and venules with consequent fall in peripheral resistance and hence MABP + venous pooling
- Despite strong sympathetic stimulation of blood vessels, the local factors (e.g. decreased O2, increased CO2, K+, adenosine) controlling vascular tone override sympathetic effect so smooth muscle relaxes.
- At capillary level, hypoxia and products of cell deterioration cause increased capillary permeability (resulting in movement of fluid from intravascular V to interstitia), causing further decrease in veinous return and MABP.
- Overall, stagnation of blood flow and formation of small clots
2) Cellular changes
- Low oxygen causes cells to work anaerobically, thus producing lactic acid
- NaCl also accumulates since the sodium pump requires more ATP than is available under aerobic conditions so the cell swells, making its membrane more permeable. Thus mitochondrial function impaired, leading to release of cell enzymes causing damage and lysis
- Cell lysis also results in inflammatory response which itself leads to increase in capillary permeability, through release of cytokines
- Local control (increased K+, decreased pH etc.) causes further relawation of arterioles and pre-capillary sphincters, resulting in TPR and BP decrease.
88
What are the signs and symptoms of shock ?
All related to low peripheral blood flow and excessive sympathetic stimulation:
♠ Thirst: due to decreased V (and increases in osmolality if occurs) detected by thirst centers in hypothalamus. Thirst center signals to posterior pituitary and ADH is released, leading to renal water retention.
♠ Skin and body temperature: cold (reflects lowered metabolic rate) and clammy skin (sympathetic mediated). If shock is due to haemorrhage, skin and mucous membranes are pale. If septic shock, body can be warm.
♠ Pulses and pressures: increase in HR (sympathetic-mediated) + weak and thready pulse (vasoconstriction and reduction in filling of vascular compartment)
♠ Urine output: Decrease in initial stages of shock (since renal blood flow decreases to maintain flow to brain and heart).
♠ Sensorium: apprehension and restlessness common, but give way to apathy as blood flow to brain decreases, which may progress to coma (coma, especially in absence of head trauma is unfavorable)
89
Is BP a good indication of perfusion ?
No, BP does not necessarily give good indication of perfusion.
90
What urine output is indicative of severe shock and inadequate renal perfusion ?
20ml/hr or less is indicative of severe shock and inadequate renal perfusion
91
If urine output a good indication of circulatory status ?
Yes, urine output gives a reasonable indication of circulatory status although flow rate increases if acute renal failure occurs.
92
What are possible complications of shock ?
♣ Shock Lung (ARDS): -Due to decreased lung perfusion and ischemia of type 2 cells + increased sympathetic stimulation (leading to venoconstriction and pulmonary oedema) + oxygen toxicity (free radical damage) + neutrophil aggregation (ultimately causes pulmonary vasoconstriction, edema, and hylaine membranes which are all bad for ventilation and gas exchange)
-This causes lungs to become stiffer (hence increasing respiratory effort and rate), and impaired gas exchange leading to hypoxaemia and hypercapnea.
♣ GI ulceration: decreased blood flow to mucosa. Common symptom is bleeding ulcers. In this way, bacteria may gain access to bloodstream and thus contribute to septic shock.
♣ Disseminated Intravascular Coagulation (DIC): formation of small clots in microcirculation. Problems with reduction of clotting factors + if thrombi become emboli
♣ Renal Damage: acute tubular necrosis. Poor urine output, salt and water overload, high plasma potassium and urea levels and, and metabolic acidosis.
♣ Multiple organ failure: life-threatening, especially in septic shock.
93
Can renal damage as a complication of shock be reversed ?
Yes, can recover if damaged: dialysis and management of shock help regenerate tubular epithelium after few days.
94
What is the onset of shock lung and GI ulcerations as complications of shock ?
Shock lung (ARDS): 24-48 hours post-trauma
GI ulceration: within hours. If bleeding ulcer, haemorrhages can have onset of 2-10 days post trauma with often no warning
95
What is treatment for GI ulcerations as a complication of shock ?
Antacids to increase pH, helps with gastric ulcers only.
96
What is the aim in treatment of shock ?
Treatment is directed towards controlling and correcting the underlying cause and improving tissue perfusion.
97
What is the treatment for hypovolaemic shock ?
Restore volume through fluid/blood/plasma expanders (latter includes dextrans and colloidal albumin solutions)
- First line is saline (0.9%)
- Plasma expanders have high MW so do no need typing and can remain in circulation for longer periods than glucose and saline solutions.
98
Why do we need to be cautions about using dextrans in hypovolaemic shock.
Because they can cause anaphylactic shock.
99
Why do we not aim to increase volume in cardiogenic shock ?
Because increasing the volume can cause the heart to become overloaded and myocardium stretched beyond optimal sarcomere length.
100
What treatment is common to all kinds of shocks ?
1) Vasoactive drugs. Capable of either constricting or dilating blood vessels. If act on alpha receptor, result in vasoconstriction. If act on beta 1 receptor, result in increased HR and contractility. If act on beta 2 receptor, result in vasodilation and relaxation of bronchioles.
101
What is the treatment for cardiogenic shock ?
Nitrates, increase arterial and veinous dilation (reducing afterload), by relaxation vascular smooth muscle.
102
Describe the structure of the wall of the trachea, and link it to its structure.
3 components:
♠ Respiratory epithelium: Pseudo-stratified columnar epithelium, lining the lumen of the trachea, contain goblet cells between ciliated columnar cells
♠ Lamina propria, deep to epithelium: CT layer, contains elastic fibres and capillaries (help warm air)
♠ Submucosa (deep to lamina propria) contains mucous glands (open by ducts on to the surface of the epithelium, help moisten air) and cartilage rings (between 16 and 20 C-shaped hyaline cartilages, help keep trachea patent.) + open end of the rings are attached by the trachealis muscle.
103
Describe the components of the wall of a bronchus.
- Respiratory epithelium lines the bronchus
- Laminar propria, deep to epithelium: CT layer, contains elastic fibres and capillaries
- Submucosa contains serous bronchial glands which lie in groups
- Cartilage becomes more irregular in shape as the airway divides. As the bronchi continue to branch, the cartilage element is reduced until it finally disappears from the wall of the bronchioles.
- Fibrous coat surrounds the bronchus.
104
Contrast the histological structure of the wall of a bronchus with that of a bronchiole. Further describe the histological structure of the wall of a bronchiole (typical bronchiole, larger bronchioles, and respiratory bronchiole).
○ The distinction between a bronchus and a bronchiole is the absence of cartilage and bronchial glands from the walls of bronchioles. Bronchioles have a diameter of less than 5mm.
○
- The wall of a bronchiole consists of a respiratory epithelial lining surrounded by bundles of smooth muscle fibres (lamina propria) and a fibrous coat rich in elastic tissue.
- The largest bronchioles: lined by a respiratory epithelium with goblet cells and cilia, but as the bronchioles branch and decrease in diameter, the epithelial cells flatten, goblet cell numbers fall and eventually disappear from terminal bronchioles.
- Respiratory bronchioles are lined by a ciliated, cuboidal epithelium. The wall is very thin and consists only of some smooth muscle cells and elastic fibres. Their wall is interrupted in some places for the openings of alveolar ducts (last divisions of the respiratory tract to contain any smooth muscle).
105
List the cell types that are found in the alveolar wall.
The alveolar wall between two neighbouring alveoli contains:
1) Rich capillary network
2) Squamous epithelial cells, which includes:
- type 1 pneumocytes (97%) in direct contact with alveolar air, and with thin cytoplasm
- type 2 pneumocytes (3%) with abundant secretory cytoplasm which include cytoplasmic vesicles containing surfactant (lowers surface tension and prevents collapse of alveoli in expiration).
3) a rich matrix of elastic fibres which support the squamous epithelial cells
106
List the factors that may affect ciliary activity in the respiratory epithelium.
- the respiratory system is lined by a delicate pseudostratified epithelium. However, some parts of the tract, which are normally exposed to direct air flow or physical abrasion have a more robust stratified squamous epithelium e.g. epiglottis, vocal folds. If air flow patterns alter e.g. with a chronic cough, the normal ciliated epithelium is lost and replaced by the more resistant stratified epithelium. This is a reversible change referred to as metaplasia. Any loss of the ciliated epithelium will impair the transport of mucus and cause congestion of the airway
- smoking increases levels of noxious gases (CO, SO2) which causes a reduction in the number of ciliated cells. Loss of ciliary action results in reduced transport of the mucous carpet
- cigarette smoke is also known to paralyse cilia
- cold dry air
- anaesthetics
- i-v barbiturate
- old age
107
Explain the relationship between the histological structure and the functions of the two parts of the respiratory system.
1) Conducting part is lined with respiratory epithelium. This enables it to moisten, clean and warm the air:
- Epithelial goblet cells secrete mucus which, along with the secretions of mucous and serous glands beneath the epithelium, create a wet surface which moistens the air and cleans it by trapping inhaled foreign particles.
- A rich, superficial vascular network within the walls warms the air.
- Hyaline cartilage in the walls of the conducting passages also provides rigid structural support which maintains the airway and ensures an uninterrupted supply of air to the respiratory part of the system.
2) Respiratory part has some smooth muscle but no cartilage in the walls of final branches. The respiratory epithelium is gradually replaced by an extremely thin squamous epithelium (facilitates the rapid diffusion of gases between the air in the alveoli and the deoxygenated blood in the pulmonary capillaries)
108
Identify places in the patient care pathway when clinical handover is required.
- patient transfer from primary (community) to secondary (hospital) care.
- patient transfer between departments within the hospital e.g. emergency medicine to medical or surgical wards
- When staff shift changes occur
- At discharge from hospital
109
Identify the system factors required to be in place for safe effective handover.
1) Protected time: Shifts need to be timed to allow a fixed crossover period for handover.
2) Key staff: There should be a clear policy stating clearly who need to attend the handover.
3) Location: A room of appropriate size to accommodate all staff required to attend, ideally close to wards
4) Format: Meeting should follow a pre-determined format to ensure efficient, succinct transfer of information.
5) Clear leadership of the handover
6) Electronic or paper based summary sheets useful for transfer of routine data allowing verbal discussion to focus on critical clinical issues.
7) Written summaries should include:
- ID details of patients handed over (at least 2 details of ID)
- accepted and referred patients to be assessed
- Accurate location of all patients
- resuscitation status where appropriate
- priority/triage coding mechanism
- current clinical problems (presenting complaint and diagnosis)
8) Verbal handover critical to highlights patients with anticipated problems, clarify medical management decisions
9) Verbal handover also needs to cover investigations completed (with results), investigations ordered and investigations needed but not yet ordered
10) Must be opportunities to ask questions and clarify
110
What are the components of the chain of infection ? Give examples for each component.
1. Infectious Agent (bacteria, viruses, fungi...)
2. Reservoir (humans, equipment, environment, food)
3. Portal of Exit (i.e. how leaves reservoir, e.g. blood and other bodily fluids, skin scales, coughing and sneezing)
4. Mode of Transmission (direct physical contact, contaminated object, air, contact with blood/bodily fluid, insect)
5. Portal of Entry (open or surgical wounds, broken skin, eyes or mouth, respiratory tract, intestinal tract i.e. ingestion)
6. Susceptible Host (underdeveloped immune system e.g. v young, decreasing immune system e.g. elderly person, drugs which lower immune system, breaks in skin).
111
Identify actions to break the Chain of Infection. Identify which components of the chain are broken in each.
1. Patient placement/assessment for infection risk (susceptible host + infectious agent)
2. Hand hygiene (mode of transmission)
3. Respiratory and cough hygiene (portal of exit)
4. PPE (Portal of entry, mode of transmission)
5. Safe management of care equipment (reservoir + mode of transmission)
6. Safe management of care environment (reservoir + mode of transmission)
7. Safe management of linen (mode of transmission + susceptible host + infectious agent)
8. Safe management of blood and body fluid spillages (portal of entry)
9. Safe disposal of waste (infectious agent + mode of transmission + portal of entry)
10. Occupation safety: prevention and exposure management (including sharps) i.e. first aid treatment following accidental exposure to blood or body fluid (portal of entry)
112
What does erythropoietin do in the body ? Where is it produced ?
Hormone which circulates in body all the time and controls the production of red blood cells.
Majority of EPO is produced in kidneys, but some is also produced in liver.
113
What factors stimulate and inhibit EPO release ?
STIMULATE EPO RELEASE:
- Hypoxia, kidney cells release increased amounts of EPO, which stimulates bone marrow cells to produced more erythrocytes from cells which are already committed to becoming erythrocytes.
- Anything causing drop in Hb levels in blood (Hb itself or RBCs) will stimulate epo release.
- Fall in PO2, or increased tissue demand for O2
INHIBIT:
- Increase in blood oxygen
- Increase in RBCs
- Increase in Hb levels
114
Which volumes/capacities cannot be measured with a spirometer ?
```
Residual V (and hence total lung capacity and functional residual V, since they both include residual V)
What RV is known, all other Vs and capacities in lungs can be calculated using a spirometer including TLC.
```
115
Describe the method used to calculate residual volume.
HELIUM DILUTION METHOD:
1) To calculate RV
-Patient asked to expire maximally
-Patient connected to a spirometer with specified volume V1, containing C1 concentration of helium (or any other inert marker gas)
-As helium-containing air is breathed in and out by patient, helium is diluted by air inside patient's lungs.
-After equilibrium is achieved, new concentration of He measured (C2).
-RV can then be measured as:
C1V1 = C2V2
where V2 is the volume of the spirometer plus the residual V of the patient, i.e. V1 + RV
Re-arrangement gives:
RV = ((C1/C2)-1) x V1
116
Describe the method used to calculate residual functional capacity.
Similar procedure to calculation of RV, but normal exhalation of patient performed before inhalation of helium-containing air.
Same calculations then performed,
RV = ((C1/C2)-1) x V1
If have the data for RV, can just calculate it because FRC = RV + ERV (latter can be obtained from spirometry)
117
List the structures through which a chest drain or needle will pass in a tension pneumothorax drainage ?
- Skin
- Superficial fascia
- Pectoralis major
- External intercostal
- Internal intercostal
- Endothoracic fascia
- Parietal pleura
118
In a tension pneumothorax, air must be aspirated from the pleural cavity. Where is the needle inserted?
For aspiration in tension pneumothorax, 2nd IC space in mid-clavicular line.
119
Describe the differences between a spontaneous and a tension pneumothorax
- Spontaneous pneumothorax: air enters pleural cavity through defect in visceral pleura. Normally, P in pleural cavity is negative but with this air entry this is no longer the case and the lung deflates due to elastic recoil of lung tissues. Depending on V of air in cavity, there may be some shift of the mediastinum. As the pleural defect heals, air is resorbed from pleural cavity and situation resolves itself.
- Tension pneumothorax: Valvular arrangement (flap of pleura) which allows air to enter pleural cavity on inspiration, but will not allow air to escape on expiration (may be associated with traumatic injuries and "sucking" wounds). With each breath, increase in V of air in thorax but with no means of escape the P increases, causing the mediastinum to shift towards the unaffected side, and reduces veinous return. Trachea may also deviate from the midline as the P pushes it towards the unaffected side.
120
How are tension pneumothoraxes dealt with ?
Aspiration (emergency)
121
Define haemothorax and chyltothorax.
♦ Haemothorax: Blood in pleural cavity
| ♦ Chylothorax: Chyle (lymph) accumulates in pleural cavity if the thoracic duct has been damaged.
122
What is the JVP an indication of ? What can you deduce from increased JVP ?
JVP is an indication of pressure on the right atrium.
If JVP is raised it could indicate a tension
pneumothorax (since it results in lowered veinous return)
123
Identify the signs and symptoms associated with a pneumothorax (including findings upon inspection, palpation, percussion and auscultation).
"-Possibly shortness of breath and raised respiratory rate
- Possibly pain
- Possibly visible cyanosis
- Patient looks distressed
- Tachycardia (if over 135, suggests tension pneumothorax)
- Possibly hypotension
- JVP may be raised (esp. in tension pneumothorax)
- Inspection: Increased use of accessory muscles
- Palpation: Decreased expansion on affected side on palpation + Trachea deviated away from affected side (esp. tension pneumothorax) on palpation
- Percussion: hyper-resonance over affected area
- Auscultation: Breath sounds reduced or absent over affected area"
124
Explain why medical need cannot be the only criterion for deciding scare organ allocation.
Because there is a relative shortage of donor organs.
125
Compare the kinds of patient characteristics that the Neuberger et al paper found that the public, family doctors, and gastroenterologists think make a patient deserving of an organ.
PUBLIC:
In decreasing order of importance, age, outcome, and time on the waiting list
FAMILY DOCTORS:
In decreasing order of importance,
outcome, age, and likely work status
GASTROENTEROLOGISTS:
In decreasing order of importance, outcome, work status, and non-involvement of alcohol.
126
Explain the ABCDE approach to assessing an unwell patient.
```
A. Airway
B. Breathing
C. Circulation
D. Disability
E. Exposure/Everything else
```
127
Define respiratory and cough hygiene.
Actions we take to contain respiratory secretions from coughing and sneezing to minimise the risk of spreading respiratory infections such as common colds and flu.
128
How far do respiratory secretions travel when you sneeze ?
5 meters +
129
Identify measures of respiratory and cough hygiene.
- Coughing and sneezing into your elbow/upper arm
- If sneezing into hand, use ABHR (and handwashing at first opportunity)
- Carry disposable tissues at all times, and washing your hands after using one
- Keep hands away from eyes and mouth if not washed hands after coming into contact with respiratory secretions
- Help patients with respiratory and cough hygiene, e.g. help them wash their hands if cannot
130
How far do respiratory secretions travel when you cough ?
Up to 2 meters
131
Describe the global distribution and incidence of asthma.
Around 235 million affected worldwide (WHO)
132
Be aware of support groups for people with asthma.
OK
133
Describe the adjustments to the respiratory system during exercise. Graph this.
- Ventilation increases in proportion to the work done: at the beginning of exercise, pulmonary ventilation increases immediately and keeps increasing until it reaches a steady state that is appropriate to the level of exercise being performed. At the end of work, ventilation rapidly falls although it may not reach normal values of pulmonary ventilation for up to an hour if the period of exercise has been intense.
- During moderate exercise, the steady state ventilation is directly proportional to the word done as measured by the oxygen consumption .
- During very severe exercise, the increase in ventilation is disproportionally large in relation to the increase in oxygen uptake, which may be a limiting factor in the capacity for exercise.
Graph of increase in ventilation with increasing oxygen uptake, with steep rise in ventilation as oxygen uptake approaches its maximum. (refer to graph in page 523 of textbook attached to guided study on effect of exercise on CVS and respiratory system).
134
What is the value of pulmonary ventilation at rest ? in exercise ?
At rest, pulmonary ventilation is about 8 L/min
| In heavy exercise, pulmonary ventilation can increase to 100 L/min and more
135
Identify the Hb saturation and oxygen content of arterial blood, and mixed veinous blood. Explain the different between the two.
- At rest, arterial blood has an Hb saturation of about 97% and an oxygen content of 19.8 mL/dL.
- At rest, mixed veinous blood has an Hb saturation of about 75% and an oxygen content of 15.2 mL/dL
- This means about 4.6 mL/dL of oxygen are extracted from each dL of blood as it passes through tissues
136
Describe the changes in blood gases that occur during exercise.
- At rest, about 4.6 mL/dL of oxygen are extracted from each dL of blood as it passes through tissues
- Overall, amount of oxygen extracted from blood into tissues increases with the intensity of exercise.
AT WORKLOADS BELOW ANAEROBIC TRESHOLD
- PO2, PCO2, pH of arterial blood all remain relatively constant
- PO2 of veinous blood draining the active muscle and that of the mixed veinous blood progressively declines as the intensity of the exercise increases.
- PCO2 of mixed veinous blood rises (from normal value of 46 mmHg). This rise in PCO2 and the associated fall in pH favor the delivery of oxygen to the active tissues (Bohr effect).
AT WORKLOADS ABOVE ANAEROBIC TRESHOLD
-Gradual reduction in PO2 and pH of arterial blood
137
Graph the changes in pH, PO2, PCO2, and oxygen contents in exercise (measured by oxygen uptake), below and above the anaerobic treshold.
Refer to graphs in page 524 of textbook attached to guided study on effect of exercise on CVS and respiratory system.
138
Identify the main phases of exercise, from a ventilation/CO perspective.
- Three phases of exercise:
1) Exercise begins, ventilation increases, and PO2 and PCO2 both change in mixed veinous blood.
2) Ventilation, CO, and partial pressures of respiratory gases in mixed veinous blood approach their steady states
3) Steady levels of ventilation, CO, Pa02, PCO2 and arterial pH are maintained. This phase is not reached until the exercise approaches its maximum sustainable capacity. In severe exercise, pH continues to fall as lactate accumulates.
139
Explain how cardiac output is matched to increased demand during exercise.
-Two main factors: commands from the brain (i.e. central command) and reflexes elicited in response to the exercise itself.
PHASE 1
Signals from higher levels of brain to regions of brainstem concerned with regulation of CVS (i.e. central command) result in:
-HR and force of contraction ↑ (potentially even before start of exercise) due to inhibition of parasympathetic activity and increase in sympathetic activity (including secretion of adrenaline from adrenal glands).
-Increased SNS activity resulting in vasoconstriction
-Reduced sensitivity of baroreceptor reflex.
PHASE 2 AND 3
- Central command reinforced by reflexes which are triggered by increased activity in the afferent nerves in the exercising limbs, and which result in increased HR and BP.
- Metaboreceptors in the exercising muscles respond to fall in extracellular pH and rise in extracellular Potassium and reinforce CV response. These reflexes are probably responsible for the matching of CO (through increase in HR/BP) to the metabolic requirements of exercise.
- The metabolites released by active muscles and the increased circulating levels of adrenaline cause a vasodilation in the arterioles which increases local blood flow. As exercise continues, body temperature begins to rise and is sensed by hypothalamic thermoreceptors. The change in activity of these receptors elicits a reflex vasodilation in the skin vessels to aid in the dissipation of the heat generated by the active muscles.
140
Explain how ventilation is increased to match demand in exercise.
Increase in ventilation during exercise is due to neural, and humoral factors.
- Neural mechanisms active respiratory muscles
- Fine tuning of ventilation to match oxygen utilization is accomplished by chemical agents
PHASE 2
- Pulmonary ventilation rises exponentially, due to composition of arterial blood acting on peripheral chemoreceptors (would explain delay in response, metabolites need to build up in exercising muscle and then transported to peripheral chemoreceptors before effect)
- Also increased neural input arising from afferent activity in the joint.
- During exercise, plasma potassium concentration is elevated in both arterial and veinous blood. Possible that the plasma potassium provides an additional stimulus to the peripheral chemoreceptors.
PHASE 3
- Ventilation is in a steady state and matched to the metabolic requirements
- Both chemical and neural stimuli are likely to be involved in maintaining the respiratory effort.
- The rise in body temperature may also contribute to the respiratory drive
- PaCO2 seems to be more closely regulated than PaO2, and CO2 eliminated is closely matched with CO2 production by exercising muscle. Evidence that relationship between ventilation and PaCO2 is reset so that there is a higher ventilation for a given PaCO2.
- Neural involvement in phases 2 and 3 of exercise is indicated by the matching of respiratory rhythm to that of the exercise.
- Afferent barrage from the muscle spindles and mechanoreceptors in muscles and joints also contributes to the activation of respiratory motorneurons.
141
Describe the stimuli that cause an increase in ventilation at the start of exercise.
Ventilation increases as soon as exercise begins, which can only be explained by a central command that is associated with the initiation of motor activity from premotor area of cerebral cortex
142
Explain whether (and why) exercise is good for you.
Yes
♠ Effects on morbidity and mortality:
-Reduces likelihood of CHD
-Lower death rate from CHD
These benefits extend to all groups including smokers and obese people.
♠ Effects on CVS:
- Lowers resting HR and increase size of heart and thickness of ventricular wall → increased EDV and SV → maintained resting CO (because lower HR)
- Maximal CO increases
- Maximal Oxygen uptake increases, and capacity of physical work is thereby increased
♠ Effects on bone:
- Greater degree of mineralisation and strength of bone
- Cartillage thicker so more compliant and has higher SA (which means pressures generated within the joint are smaller for given task)
♠ Effects on muscle:
- Initially (beginning of training), force generated of muscle fibers increases without increase in their diameter (i.e. due to improvement in recruitment of motor units during the performance of a specific type of exercise)
- Then, CT mass and muscle mass hypertrophy (diameter of fibers increase but same number)
- Increased mass of tendons and CT of muscles improves their ability to transmit the force generated by muscle fibers to skeleton
- In dynamic exercise (e.g. running), progressive increase in the capillary density of the muscle with the duration of training, and a consequent improvement in the transfer of oxygen from the blood to the tissues.
