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PHYSIOTHERAPY > HUMAN FUNCTIONING CARDIORESP > Flashcards

HUMAN FUNCTIONING CARDIORESP Flashcards

1
Q

What are the key features of the upper respitory tract?

A

Starts at the nostrils and ends at the larynx
The nasal cavity is ciliated and lined with mucous producing epithelial cells
Muscles are under voluntary and involuntary control
The pharynx (throat) is cone shaped muscular passageway extending from the base of the skull to C6
The larynx (voicebox) is a cartilaginous passageway from the larynx to the trachea
The epiglottis is a flaplike projection at the upper part of the larynx

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2
Q

What are some of the key functions of the upper respiratory tract?

A

Filtering, warming and moistening inhaled air
Protective - smell, protection of infections (tonsils), reflexes (cough, gag, sneeze), mucus production
Speech
Airway patency - lowest resistance to flow in the respiratory tract (pharynx most vulnerable)

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3
Q

What are the key features of the lower respiatory tract? Trachea

A

Tubular structure supported by C shaped cartilaginous rings
Extends from the larynx to the bronchi
Lined with ciliated epithelium and mucous producing goblet cells - mucociliary escalator
Contains sensory receptors

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4
Q

What are the key features of the lower respiratory tract? Bronchi and bronchioles

A

Right and left main bronchus
Right side is more vertical
Bronchi branch into secondary and tertiary bronchioles
Bronchioles diameter is less than 1 mm
No goblet cells in bronchioles (they have clara cells that secrete surfactant)
Increasing levels of bronchial smooth muscle (bronchoconstriction)
Terminal bronchioles lead to alveoli.

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5
Q

What are the key functions of the lower respiratory tract?

A

Air conduction, air distribution and airflow control (resistance to airflow)
Filtration
Protection (cartilaginous rings)
Cough reflex
Gas exchange (terminal bronchioles only)

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6
Q

What are the key features of the lungs?

A

Right lung has three lobes, the left lung has 2 lobes to accomodate the heart
Surrounded by a pleura (inner layer is visceral, outer layer is parietal)
Recieve rich vascular supply from pulmonary circulation
Contains millions of alveoli which are interconnected allowing collateral ventilation

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7
Q

What are the key functions of the lungs?

A

Gas exchange
Respiratory defence
pH regulation
Ventilation perfusion matching

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8
Q

What are the key features of the thorax (joints)?

A

Costovertebral
Costotransverse
Sternocostal
Costochondral
Interchondral

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9
Q

Applied anatomy of the ribs?

A

Ribs 1-3 are the hardest to break so signify significant degree of trauma if damaged
Ribs 4-10 are typically the most vulnerable
Ribs 11-12 are more mobile and therefore more difficult to break
Rib fractures may be pathologic as a result of cancer metastasis from other organs
Rib fractures due to stress in athletes
Rib fractures due to severe cough
Children are less likely to develop rib fractures due to their ribs being more elastis, so signs of significant trauma

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10
Q

Describe the anatomy of the diaphragm?

A

Inserts via a central tendon which has partial attachments to the pericardium
3 origins (sternal, costal and lumbar)
Right and left phrenic nerves (C3 through C5) - C 3,4,5 keep the diaphragm alive
Attaches xiphoid process, lower 6 ribs and their costal cartilidge, and upper 3 lumbar vertebrae
Inserts - central tendon

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11
Q

What are the accessory muscles of breathing?

A

Sternocleidmastoid
Scalene
Trapezius
Latissimus dorsi
Seratus anterior
Pectoral muscles

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12
Q

What are the key functions of the thorax?

A

Bae for muscle attachment (stability)
Protection of viscera (strength)
Spinal stability and load bearing (stability)
Role in ventilation (stability and mobility)

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13
Q

How does the ventilatory pump link to the CNS?

A

The respiratory centre is located in the medulla oblongata and pons, and is involved in the minute-to-minute control of breathing
Medulla DRG - initiates inspiration
Medulla VRG - initiates expiration
Pons potine pneumotaxic - limites inspiration
Apneustic centre - antagonist to pneumotaxic centre so promotes inhalation

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14
Q

When can dysfunction of the respiratory system occur?

A

When there is a loss of balance in:
Capacity:
- muscle atrophy/fatigue
- Kyphoscoliosis
- Malnutrition
- Altered mechanics
Load:
- Airway narrowing
- airflow obstruction
- increased O2 demand
- Reduced lung volume

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15
Q

When can the functional residual capacity be reduced?

A

Reduces with:
age
supine position
surgery
obesity
atelectasis
contact injuries eg winded

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16
Q

What is lung compliance?

A

How much the volume of the lungs can change for each unit change in pressure (the change in volume in the lungs for a given change in pressure)
Measure of elasticity
(think of balloon demonstration for alveoli, harder to add air initially - relatively small change in volume for a big change in pressure)
Factors that effect compliance:
- position
- age
- obesity
- lung diseases
eg atelectasis, empheysema
The combines lung - chest wall system is at equillibrium when lung volume is at functional residual capacity, which is the remaining lung volume after tidal volume is expired.

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17
Q

What is the ventilation perfusion ratio?

A

Ventilation Refers to the amount of gas that moves into and out of the avleoulus that can participate in gas exchange
Perfusion (Q) refers to the amount of blood that moves past the alveolus that can participate in gas exchange
Want the V:Q to be as close to 1:1 as possible
If ventilation drops or decreases, you want perfusion to do the same
Decreased oxygen in the alveolus (eg due to blockage in the alveolus), results in decreased blood flow due to (pulmonary arterial) vasocontriction. This decreases perfusion.
A drop in CO2 due to a bloacge in the arteriole, causes the bronchioles to constrict, which reduces ventilation (matches the drop in perfusion)

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18
Q

What is pH?

A

Potential of hydrogen
0-14 acidity to alkalininity
Critical parametre in humans 7.35 - 7.45
Influences cellular function, enzyme function, release of oxygen from haemoglobin, protein stability
pH less than 7 (severe acidosis) and pH greater than 7.8 is severe alkalinosis which is likely to be incompoatible with life

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19
Q

Homeostatic balance of PH in the lungs and kidneys?

A

Carbon dioxide and water form carbonic acid which is in equillibrium with bicarbonate and hydrogen ions. A change in either side affects the direction of the reaction.
The lungs excrete or retain carbon dioxide by altering respiration
The kidneys excrete hydrogen ions or excrete bicarbonate in urine

Buffers include:
Bicarbonate
Phosphates
Plasma proteins
Haemoglobin

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20
Q

What is bicarbonate and base excess?

A

Reflects the renal/metabolic component of acid/base balance
Base excess estimates the degree of acidosis/alkalosis. Refers to the amount of acid that is needed to restore pH to normal.
Less than 22 is metabolic acidosis
Greater than 26 is metabolic alkalosis

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21
Q

What is PaCO2?

A

The partial pressure of carbon dioxide in arterial blood
Reflects the adequacy of ventilation
Increased = hypoventilation (hypercapnia/acidosis)
Decreased = hyperventilation (hypocapnia/alkalosis)

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22
Q

What is PaO2?

A

Partial pressure of oxygen in arterial blood
- Hypoaxemia - deficiency of O2 in arterial blood
- Hypoxia - deficiency of O2 at tissue level
Has no influence on pH.

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23
Q

What are the 4 main arterial blood gass derangements?

A

Respiratory acidosis - increase PaCO2
Respiratory Alkalosis - Decreases PaCO2
Metabolic acidosis - decreased bicarbonate
Metabolic alkalosis - increased bicarbonate

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24
Q

What is acute respiratory acidosis?

A

Arises when effective alveolar ventilation fails to keep pace with the rate of CO2 production.
Hypoventilation (shallow breathing or too slow so co2 levels rises) eg CNS depression phneumonia
Decrease in PH and increase in pressure of co2
May require assisted ventilation

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25
Q

What is acute respiratory alkalosis?

A

Caused by hyperventilation eg anxiety, pain, heart failure
Increase in pH and decrease in pressure of carbon dioxide

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26
Q

What are some compensations for respirtory disorders?

A

Chronic respiratpry acidosis - HCO3 and BE levels increase (less excreted in urine to reduce acidity)
Chronic respiratory alkalosis - HCO3 and BE levels decrease (more excreted in acidity)
Metabolic acidosis - hyperventilation to reduce PaCO2 (reducing acid in the blood)
Metabolic alkalosis - hypoventilation to increase PaCO2 (increases acid in the blood)

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27
Q

What is asthma?

A

Chronic inflammatory disease of the respitory system characterised by reversible airflow obstructions, characterised by bronchial hyperresponsiveness and bronchial inflammation.
The airways have hypertrophied smooth muscle which contract spontaneously or in response to a triggering factor, hypertrophy of the mucus glands, odema of the bronchial wall, infiltration of white blood cells

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28
Q

What are the triggers of asthma?

A

Extrinsic asthma (allergic) - pollen, dust, pests
Intrinsic asthma - (non allergic), viral infections, cold air, GERD (acid reflex), medication eg beta blockers, NSAIDS
Childhood exposure to second hand smoke increases risk

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29
Q

What are the symptoms of asthma?

A

Persistent dry cough
Shortness of breath
Chest tightness (tight bronchioles)
Expiratory wheezes (hard for air to get out of the lungs)
Hyperresonant lung percussion

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30
Q

Diagnosis of asthma?

A

For patients over 5:
Typical clinical features of asthma, demonstration of reversible bronchoconstriction eg pulmonary function tests, spirometry (might struggle to exhale deeply, forced expiration is less)

Asthma is reversible so symptoms might not always show. In this case can do a bronchial provocation test that provoke bronchoconstriction eg melacholine test then spirometry or exercise then test (risk)

COPD will also show similar results in spirometry. COPD will usually have baeline obstruction ALL the time as opposed to SOME of the time. Can also do the bronchodilation reversibility test - albulerol will cause bronchodilation so spirometry will increase. In COPD patients there will be no/less change.

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31
Q

How is asthma classified?

A

Intermittent asthma - symptoms less than twice per week, wake up less than 2 times per month, use of SABA less than 2 days per week. Lung function - forced expiratory volume less than 80%. Treated with SABA inhaler eg albuterol. Rescue inhaler.

Persistent asthma: mild persistent, moderate persistent and severe persistent asthma
Mild persistent - more than twice per week, waking up at night 3-4 times per month. FEV1 greater than 80%
Moderate persistent - symptoms daily, waking up more than once per week. FEV1 - 60% - 80%
Severe persistent - daily symptoms, waking up every night, extreme limitation. FEV1 less than 60%.

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32
Q

Treatment for persistent asthma?

A

Mild persistent: daily therapy, low dose ICS eg budesonide. Rescue therapy SABA
Moderate perisstent: daily therapy with low dose ICS and formoterol inhaler (daily and rescue). Or ICS and LABA or ICS and LAMA or ICS and LIRA
Severe persistent - daily therapy ICS LABA and LAMA

Bronchodilators
Steroids
Management of breathlessness
Management of infections
Management of trigger factors
Management of exacerbations

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33
Q

What is COPD?

A

An iireversible obstructive lung disease
Risk factors - smoking for more than 30 years due to chronic destruction of lungs, exposure to chemicals, fumes and smoke

2 types:
emphysema (pink puffer) - difficulty breathing, damage to alveoli loss of lung elasticity and inflation. loss of surfactatnt so loss of recoil. air trapping
PINK - pink skin and pursed lip breathing, barrel chest, no chronic cough, keep of tripoding.
Symptoms - Dyspnea at rest, weight loss, prolonged expiration, clubbing fingers
Complications - frequent infections, risk for pneumothorax
Enlarged air spaces and alveoli distal to the bronchial, and destruction of the walls of the air spaces. Loss of elastic tissue leads to floppy airways that collapse as the person breathes out. Makes it hard for them to breathe in as the inspiratory muscles have to overcome this positive pressure. Also causes CO2 to get trapped in the airways, so O2 can’t get into the blood.

and chronic bronchitis (blue bloater) - inflammation of the bronchi, excessive musus production, reaccuring infectiod and hacking cough
BLUE - big and blue skin (cyanosis due to hypoxia (low oxygen)), obese, increase in red blood cells in the body which can cause blood clots due to vasocontriction (must report this), long term chronic cough and sputum, unusual lung sounds (crackles and wheezes), edema peripherally
Right side heart failure rocks the body with fluid = edema and weight gain

Decreased O2 saturation levels 88-93%

Arterial blood gays- low oxygen and height carbon dioxide
Low paO2 = hypoxia
high paco2 = hypercapnic
Will generally show increased acidosis (high co2 puts the body into acidocic state)

Use biPAP for hypercapnia (not inhaler)

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34
Q

What is pleuritic chest pain?

A

Inflammation of the pleural lining after a chest infection, sharp pain worsen by breathing and coughing

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35
Q

Define dyspnea

A

A difficulty breathing occuring at a level of activity where it would not be expected
Some problems with identifying breathlessness include:
No specialised receptors
No identified area of the cortex
No single easily identifiable stimulus (metabolic work, increased airways resistance, change in ABG’s or weak/fatigued muscles)
Very subjective, sensation - based on experience and personality

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36
Q

What is tachypnoea?

A

Rapid breathing

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37
Q

What is hyperventilation?

A

Ventilation in excess of metabolic requirements

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38
Q

What are some of the different types of breathlessness?

A

Orthopnoea - short of breath when lying flat
Paroxysmal nocturnal dyspnoea (PND)
Short of breath at rest (SOBAR)
Short of breath on exertion (SOBOE)

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39
Q

What are some of the pathophysiologicl basis of dyspnea?

A

Added load on the mechanics of breathing eg during exercise
Pshycogenic factors
Weakness or fatigue of respiratory muscles
Low CO2 or ischaemia
Increase in ventilatory requirements
Cardiovascular and respiratory deconditioning
Blood gas abnormalities
Perfusion limitation

40
Q

What are some possible mechanisms for the sensation of breathlessness?

A

Motor command theory - sense of effort: increases whenever the central command to the respiratory muscles must be increased eg when the muscle load is increased, when muscles are weak or to increase lung volume

Length-tension theory - the brain expects a certain pattern of ventilation and deviations from this pattern can lead to the sensation of dyspnea.

Mechanoreceptors - upper airway receptors may modify the sensation, lung receptors (irritant receptors) may give the sensation of tightness or constriction. Chest wall receptors: a disturbance between the force generated by the respiratory muscles and the resulting change in muscle length and lung volume may lead to dyspnea

Pshychological/Emotional factors

Chemoreceptors - hypoxia and breathlessness are not necesarily related, hypercapnia has been shown to cause dyspnoea

41
Q

What are some obstructive classifications of cardiorespiratory disease?

A

Chronic obstructive
Pulmonary disease
COPD
Asthma
Cystic fibrosis
Bronchiectasis
Primary ciliary
Dyskinesia

42
Q

What are some restrictive classifications of cardiorespiratory disease?

A

Intersitial lung disease
Neuromuscular disease
Pleural effusion
Pneumothorax
Pneumonia

43
Q

What are some symptoms of COPD? OBSTRUCTIVE8

A

Shortness of breath
Chronic cough
Poor exercise tolerance
Evidence of airway destruction
Over inflated lungs
Impaired gas exchange

44
Q

Explain different types of airway obstruction?

A

Within the airways lumen - partly occluded by the presecen of excessive secretions as in chronic bronchitis, bronchiectasis and cystic fibrosis (reversible as airways can be cleared of secretions)

The airway wall - partly occluded because of a decrease in the size of the airway wall, might be due to increase in contraction of bronchial smooth muscle eg asthma, hypertrophy of the mucous glands eg chronic bronchitis or inflammation (reversible if bronchspasm or inflammation, irreversible if due to scarring)

Outside the airway - partly occluded due to destruction of the lung parenchyma (lung tissue) may cause loss of elasticity eg emphysema. (iireversible if changed in airway structure take place)

45
Q

How do airways collapse due to COPD?

A

The bronchioles become less elastic and narrow when exhalation occurs. This reduced elasticity and inflammatory process causes the airways to narrow and collapse. A a result, CO2 gets trapped in the airways and prevents O2 from getting into the blood. This can cause mucus to also become trapped, which can lead to atelectais (airway collapse) and is a source of infection.

46
Q

What are the classifications of emphysema?

A

Centriacinar/Pentrilobular:
Predominantly respiratory bronchioles
More severe in upper zones
Clasically seen in smokers
Usually in association with chronic bronchitis

Panacinar/Panlobular:
Involved the whole ancinus (bronchioles, alveolar ducts and the alveoli sacs)
Uniform throughout the lung or more severe at the bases
Antitrypsin deficiency and early development of panacinar emphysema

Emphysema is characterised by destruction of alveoli so hat there is a permenant dilation of airspaces. Bulla are large dilated airspaces that bulge out from beneath the pleura.
Categoriased as anythingt hat degrades the alveoli eg bronchitis, asthma and TB

47
Q

Summary of emphysema? OBSTRUCTIVE

A

Anything that degrades the alveoli walls, eg bronchitis, asthma and TB, heavily polluted air and prolonged exposure to certain dusts and genetic makeup
Reduced elasticity and inflmmatory process causes the airways to narrow and collapse (due to an antitrypsin deficiency which causes a loss of elastin and alveolar wall destruction
Results in carbon dioxide gets trapped in the airways and prevents oxygen from getting into the blood
There is no cure for emphysema
Permenant dilation of lung spaces (bulla are large dilated airspaces that bulge out beneath the pleura

48
Q

Pink puffer vs blue bloater?

A

Pink puffer: maintains normal blood gases, severe breathlessness, weight loss enxiety, physical tension, over expanded chest (emphysema??

Blue bloater: not normal blood gas levels, less breathless, nocturnal hypozmia, bloated, double the mortality of pink puffer, chronic cough, normally long term smoker, signs of fluid retention eg swollen ankles

49
Q

What is chronic bronchitis? OBSTRUCTIVE

A

Characterised by an excessive production of mucus in the bronchial tree

50
Q

How can COPD lead to heart failure?

A

In chronic hypoxia the airways constrict as they detect low oxygen levels
This causes an increased blood pressure in the pulmonary circulation
The heart has to contract more strongly to pump the blood around the body
The right ventricel is not as muscular as the left so hypertrophies to compensate
Causes left ventricle to also hypertrophy, and the ventricles begin to fail
Results in oedema (build up of fluid)
Polycythemia also occurs but increases the tickness of blood which increases resistance to circulation

51
Q

What is some of the treatment for COPD?

A

Avoidance
Antibiotics
Anti-inflammatory drugs
Bronchodilators
Pulmonary rehab (exercise)
Coping strategies for breathlessness
Chest clearence
Long term oxygen therapy
Assisted ventilation

52
Q

What is cystic fibrosis? OBSTRUCTIVE

A

Affects electrolyte and water transport in and out of body cells. This allows too much salt and not enough water into cells causing a thick sticky mucus.
The function of chloride channels are affected, which results in cells that line the passageway of the lungs, pancreas producing unusually thick and sticky mucus.
Mucus leads to bacterial infections, which leads to progressive lung damage as dying neutophils release DNA whose strands bind together and further thicken the mucus.

Clinical features:
Cough and mucus, bronchiectasis (widening of the lungs airways), delayed puberty or infertility in males, breathlessness, pleuritic pain, pneumothoraces, malnourishment

53
Q

What is primary ciliary dyskinesia? OBSTRUCTIVE

A

An uncoordinated cilia beat (the cilia waft in different directions). Leads to excess secretions and recurrent infections

54
Q

What is bronchiectasis? OBSTRUCTIVE

A

Chronic irreversible and distortion and dilation of the bronchi
Associated with persistant lung infections, foreign body inhalation, CF, TB, inhalation injury

The airways tend to collapse, causing a pressure drop along floppy airways, and debris tend to remain in dilated sacs, so cough clearence is greatly impaired.

Increase airway resistance.

Airways become colonised with bacteria/

(not a final diagnosis, but a common pathway of several conditions, eg developed by CF and COPD patients).

Clinical features:
Voluminous amounts of sputum
Foul smelling and haemoptysis
Fatigue, loss of eppetite
Dyspnoea
Chronic lung infection
Possibility of heart failure

Antibiotics can help control infection, and steroids can asisst inflammation. Mucolytics help thin mucus. Surgical resurection or transplant may be needed.

55
Q

What are restrictive lung disorders?

A

Characterised by decreased lung volume, poor lung compliance, and increased work of breathing.

Causes: shrunken lung tissue, compressed lung tissue within the chest wall, compressed lung tissue by the chest wall, reduced ability to expand the lung.

56
Q

What is interstitial lung disease?

A

Disease that affect the supporting structures of the lunngs rather than the airpspaces
Inflammatory changes lead to alveolitis fibrosis, thickening and remodelling of lung tissue leading to shrunk and stiff lungs
Thickening of the interstitium of the alveolar walls
Increased work of breathing and impaired gas exchange
Covers 200 disorders

57
Q

What are some examples of interstitial lung disease?

A

Fibrosing alveolitis/pulmonary fibrosis - crackles heard, finger clubbing potential, maybe cor pulmonale: cause is unknown or spontaneous

Lung fibrosis - the fibrous lung tissue scars and reduces the elastic properties. Small lung volumes requiring abnormally high pressure to inflate. Airways narrow when lung volume reduces. Bronchioles dilate and are surrounded by thick scar tissue: hypoxia, impaired diffusion, shallow breathes

58
Q

What is some treatment for interstitial disease?

A

Steroids -often fibrosis is established so use is limited
Collagen inhibitors
O2 therapy - needed in later stages, especially when exercising
Non-invasive ventilation - invasive is avoided as this can further reduce lung compliance
Lung transplant

59
Q

What are some disorders within the chest wall?

A

Pleural effusion - excess fluid in the pleural cavity disturbing hydrostatic pressure, reduces expansion. If the drained fluid is straw colour indicates due to heart failure, cloudy indicates malignancy

Pneumothorax - trauma, need to restore negatuve pressure in pleural space. Air will enter the pleural space in inspiration but cannot escape during expiration. In a tension pneumothorax, air from ruptured lung enters pleural cavity, building up pressure, compressing lung and displacing organs to the other side of the chest.

Pleurisy - inflammation of the pleural layers due to infection, associate with pneomonia. Can hear pleural friction rub on ascultation, sharp pleural pain

60
Q

What are some disorders of the thorax and musculature?

A

Scoliosis
Kyphoscoliosis
Ankylosing Spondylitis

Reduces chest capacity
Prone to chest infections/pneumonia
May need non invasive ventilation
Thoracic mobility exercises
Mortality due to respiratory failure

A distorted spine increases work of breathing because of reduced chest wall compliance, micro atelectasis and altered alveolar surface tension.

Resiratory muscles may also be forced to work inefficiently.
An effective cough might also be difficult.

61
Q

What are neuromusclar respiratory disorders?

A

Weak inspiratory muscles restrict expansion eg polio
Sputum clearence is impaired due to weak cough

62
Q

What are parenchymal disorders?

A

Infective or chemical agents inflame lung tissue and then fill alveoli with extudate eg pneumonia

Dry cough that can become productive of purulent and maybe blood stained

63
Q

Describe pneumonia?

A

Bacterial, viral or fungal infection in the alveoli
Bronchi become inflammed and fill with fluid
Flu like symptoms
It is an acute respiratory tract infection
The lung fills with liquid and solidifies

Aspiration pneumonia occurs when there is an inhalation of any unwanted substance into the lungs. It is common in neuromuscular disease due to poor gag reflex

64
Q

what is Tuberculosis?

A

Caused by bacteria, contagious spread through the air, propelling TB germs, can lie dormant for years until immune system is weakeened
Symptoms: fever, night sweats, persistent cough, weight loss and haemoptysis. Disease causes damage to the lung tissue and pleural effusion may develop which leads to severe breathlessness
The infection can spread to the blood stream and cause sepsis

65
Q

What is lung absecess?

A

Necrosis (death of cells) of pulmonary tissue and the formation of cavities. Oral bacteria, fould smelling secretions and daemoptysis.

66
Q

Describe the types of lung cancer?

A

Small cell lung cancer: highly malignant, most viscious and rapidly spreading
Non-small cell:
- Squamous cell carcinoma: most common type, develops in the cells which line the airways, most often caused by smoking.
- Adenocarcinoma: develops from the cells which produce mucus in the lining of the airways

Large cell carcinoma: large, rounded cells, occurs in peripheral lung tissue

Smoking is the main cause. Air pollution, asbestos, TB, COPD, Radon exposure and cerrain occupations increase risk

Symptoms: haemoptysis, pleural effusion, hoarseness of voice, chest infections, pain and cough, anaemia, weight loss and fatigue.

Mesotheliaoma: cancer that forms in the mesothelium, caused by asbestos.

67
Q

What is obstructive sleep apneoea?

A

Totoal blockage of the throat as the muscles relax
Apnoea (lack of breathinn lasting 10 seconds)
Obesity is the main risk factor
Snoring and interrupted sleep
Daytime sleepiness, headaches and poor memory
May require nocturnal ventilation

68
Q

Why is the CVS system important?

A

Oxyegn and nutrient transport
Waste removal - ensures elimination of metabolic byproducts
Thermrugulation
Supports the immune system - transport white blood cells to initiate immunological response.
Hormone transportation
pH Level Maintainence
Blood pressure regulation
Nutrient storage and distritbution

69
Q

Describe the anatomical location of the heart?

A

Encased in the mediastinum
Aortic arch sits level with 1st rib
The apex sits between 4th and 5th ribs on the left side of chest

70
Q

Describe cardiac muscle?

A

Small striated and branching with single nucleus
Each cell connected to neighbour by intercalated discs - a synytium. Allows passage of electrical currents and small molecules between adjacent cells (controlled by the metabolic state of cells)

Involuntary control
Involuntary contractions that are coordinated and rhythmed
Capacity to contract in a rythmic manner in the absence of external stimuli.

71
Q

Describe heart valves?

A

4 heart valves
- tricuspid
- pulmonary semilunar
- mitral (bicuspid)
- aortic (semilunar)

Purpose is to prevent backflow of blood and to keep blood flowing in one direction.

72
Q

What are the characteristics of blood?

A

Viscous
Temperature is 38 degrees
pH is 7.35 - 7.45 (slightly alkaline)
Salt concentration is 0.9%
8% of total body weight
- male av 5-6 litres
- female av 4-5 litres

73
Q

What are the components of blood?

A

Fomed elements (cells and cell like structures) make up 45%
Plasma (liquid that contains dissolved substances) is 55% of blood

74
Q

What is the circulatory system?

A

A continuous system
- systemic circulation, ox blood from heart to body
- pulmonary circulation, blood from heart to lungs

Blood flows with almost no resistance in larger vessels
Considerable resistance exists in smaller vessels (poiseuilles law)

75
Q

Describe systemic and pulmonary circulation?

A

Both include:
- a distributary system
- a variable resistance system
- an exchange system
- a collecting system

76
Q

What is the role of the systemic circulation?

A

Distributes metabolites and oxygen
Collect waste products and carbon dioxide
Regulation of BP
Pulsatile through arterioles
3/4 of blood volume found in systemic circulation
2/3 of blood in veins

Involved in thermoregulation and distribution of hormones

77
Q

What is the role of the pulmonary circulation?

A

Respiration; gas exchange
Reservoir of blood available to L side of heart to allow increase in CO
A filter for small thrombi

78
Q

Describe the flow of blood through the cardiac circuit?

A

Right atrium - deox blood from body enters the heart
Right ventricle - the right atrium contracts and forces blood into right ventricle
Pulmonary artery - right ventricle contracts and supplies the lungs with deox blood via pulmonary artery
Lungs - blood receives O2 in the lungs and releases CO2.
Left atrium - ox blood returns to the heart via the left atrium.
Left ventricle - left atrium contracts and forces blood into the left ventricle
Aorta - the left ventricle contracts and distributes oxygenated blood via the aorta throughout the body.
Tissues - nutrients and oxygen are transported to the tissues of the body.
Vena Cava - the cycle is restarted when deox blood returns to the heart via the superior and inferior vena cava.

79
Q

Define systolic?

A

Pertaining to the systole aspect of the cardiac cycle (heart contraction)

80
Q

Define diastolic?

A

Pertaining to the diastole aspect of the cardiac cycle (heart relaxation)

81
Q

Define end diastolic volume (EDV)?

A

Volume of blood in the ventricle at the end of diastole

82
Q

Define end systolic volume (ESV)?

A

Volume of blood in the ventricle at the end of systole.

83
Q

Define Cardiac Output (CO)?

A

Volume of blood pumped by the heart in one minute.

84
Q

Define stroke volume (SV)?

A

Volume of blood pumped by the heart each contraction.

85
Q

What is the cardiac cycle?

A

The period from the end of one contraction of the heart to the end of the next

Each cycle is generated by a spontaneous action potential (AP) generated by the Sinoatrial Node.

86
Q

Describe cardiac action potentials?

A

A brief change in voltage (membrane potential) across the cell membrane of heart cells
Action potential arises from specialised pacemaker cells
These cells have autonomic action potential generation capability and are found in the SA node in the right atrium
The action potential passes along the cell membrane, causing the cell to contract, and is essential for stimulating and maintaining regular contractions of the heart.

87
Q

What are pacemakers?

A

Specialised groups of cells within the heart capable to spontaneously generate action potentials.
- SA node and AV node
- Purkinje fibres

Atrial and ventricular muscle cells have high resting potentials and show no spontaneous activity.

88
Q

Describe the action of the AV node.

A

The AP spreads rapidly through both atria
Contraction of atrial muscle
Stimulation of the AV node (a delay of 0.1 seconds at the AV node allows ventricular filling.

89
Q

Describe ventricular diastole.

A

Atrium is still in diastole
Blood flows from venous system into atrium increasing pressure
Atrial pressure is greater than ventricular pressure so AV valve opens
Blood flows passively into ventricle so volume increases

The SA node fires
The AP spreads throughout the atris and the atria contract (atrial systole)
Increased atrial pressure so more blood into the ventricles
Ventricular pressure increases

AV valves open trhoughout atrial systole
Ventricular contraction at end of ventricular diastole
Volume of blood in ventricles known as end diastolic volume.

90
Q

What is Isovolumetric Ventricular Contraction?

A

After AV valve closure and before aortic valve opening. The ventricle is effectively a closed cell. (first stage in the cycle)

Isovolumetric Ventricular Relaxation is the second time all valves are shut.

91
Q

What is exercise physiology?

A

The study of the body’s response to any form f physical activity or exercise
Aute exercise
Chronic exercise eg repeated bouts
Response to environ
Response if different pops

92
Q

What is the a-vO2 difference?

A

Arteriovenous oxygen difference is the difference in the oxygen content of the blood between the arterial blood and venous blood. It is a good way of seeing how much O2 is delivered and used by muscle.

93
Q

Define VO2 max

A

The highest rate of oxygen consumption attainable during maximal or exhaustive exercise.

94
Q

Define tidal volume

A

The amount of air that moves in or out of the lungs with each respiratory cycle (normal breath)

95
Q

What is the average respiratory rate?

A

12-15 breaths per minute at rest

96
Q

What is concurrent training? What is the average pulmonary (minute) ventilation?

A

The process of inspiration and expiration, for a young adult averages 5-6 litres per minute.

Pulmonary ventilation = respiratory rate x tidal volume.

97
Q
A

PHYSIOTHERAPY (14 decks)

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