Download History of fall

FALL = a sudden, unintenstional change in position causing someone to land at a lower level
– other than due to paralysis, seizure or overwhelming force
Recurrent falls are defined as those occurring at least 3 times a year.
 Understand epidemiology of falls in the elderly.
Frequency:
>65 years: 30% per year
> 70 years: 35% per year
>75: 40% per year
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50% of nursing home residents fall.
Injuries due to falls are the most common cause of mortality in people >75 in the UK.
Other groups - young children and athletes - also have high incidence of falling but are less
susceptible to injury (have less chronic diseases and age-related physiological changes) and
recover more quickly.
For a primary care trust and local authority with a population of 320,000:
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15,500 will fall each year; 6,700 people will fall twice
2,200 will attend accident and emergency departments or minor injuries units
A similar number will call an ambulance
1,250 will have a fracture of which 360 will be hip fractures
 Identifies and manages factors contributing to recurrent falls/collapse.
DAME: Females > males
D rugs incl alcohol
A ge related cahnges (gait, sensory, vision impairment)
M edical (CVD, parkinson’s disease)
E nvironental obstacles
Internal risk factors
Individual characteristics
 Female gender
 Low weight
 Low muscle strength
 A history of fall in the last year
 Age (>80 years)
 Use of an assistive walking device
 Dependency in activities of daily living
Medical conditions
 Visual impairment: acuity, contrast sensitivity,
depth perception, and dark adaptation decline
with age. ALSO cataract, glaucoma, macular
degeneration, Central retinal artery /vein
occlusion can impair vision
 Orthostatic hypotension
 Diabetes mellitus
Cognitive/psychiatric conditions
 Central processing decline: e.g. delirium,
dementia
 Depression
 Impaired cerebral perfusion by:
o Diuretics (esp. if dehydrated)
o Antiarrhythmics
o Antihypertensives (especially
vasodilators)
Drug causes
 Alcohol abuse
 Sedative medication, including
hypnotics (may impair co-ordination
and cause falls). There is a particular
risk of falls in agitated patients with
cognitive impairment.
 Confusion particularly from
psychotropic medication may
increase the risk of falls.
 Polypharmacy - the scope for
interactions and other effects is
increased.
 Reduced alertness or slow central
processing by:
o Analgesics (especially opioids)
o Psychoactive drugs (especially
antidepressants, antipsychotics,
and benzodiazepines)
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Mobility problems
 Mobility limitation
 Balance deficit
 Gait deficit
 Arthritis
External risk factors
 Inappropriate footwear e.g. slippers
 Incorrect use of walking aids
 Pets underfoot
 Trailing electrical cables
 Older housing needing repairs
 Poor lighting, especially near stairs
 ‘A lifetimes clutter’
Vestibular damage by:
Aminoglycosides
Lood diuretics (high dose)
o
o
Orthostatic hypotension caused by:
o Diuretics (can cause dehydration
and may cause urgency and falls)
o Vasodilators (including calciumchannel blockers and nitrates)
o Alpha adrenergic blockers
o Angiotensin-converting enzyme
(ACE) inhibitors
o Alpha-blockers
o Phenothiazines
o Tricyclic antidepressants
o Levodopa
o Bromocriptine
o Betablockers
o Insulin
Unfamiliar environment e.g. new home,
hospital
 Walking while talking or being distracted by
multitasking and failing to attend to an
environmental hazard (e.g. a curb or step)
 Rushing to the bathroom (especially at night
when not fully awake / poor lighting), and
rushing to answer the telephone.
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 Relevant history including from witness of fall/collapse
 Drug and alcohol history
History of fall
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Was the fall an isolated event or one of many? If many, is there any pattern? How often do they
occur? Are they getting more frequent? Does there seem to be any common precipitating factor?
Before
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What caused the fall?
o
Sometimes the fall is attributed simply to tripping over a loose rug or a trailing electric cable.
This is not a medical problem but requires a home safety assessment with a visit by a health
visitor.
o
Or was it loss of balance? ‘Faint’?
o
If history suggests tripping, ask about eyesight and when last assessed by an optician.
What was the patient doing at the time?
o
Was it something involving exertion? Was the patient in an emotional situation?
o
Did it involve looking up? Extending the neck to look inside a low cupboard or to do high
dusting risks vertebrobasilar insufficiency.
o
Older people should be discouraged from climbing on chairs or ladders since they are more
likely to fall in these situations and will fall further, incurring more serious injuries.
o
Position (e.g. lying or standing), and, if standing, for how long. Postural hypotension usually
occurs on suddenly getting up from sitting or from lying in bed - typically, on getting out of
bed to go to the toilet in the night.
o
Micturition syncope affects men, usually as they stand up at the toilet, attempting to pass
urine nocturnally.
o
Does the patient have a sleep disorder? These are reasonably common in older people and
may contribute to the risk of falling.
Associated symptoms (e.g. palpitations, shortness of breath, chest pain, vertigo, light-headedness,
nausea, sweating, blurred or tunnel vision, tingling of lips or fingertips)
During
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Was there any loss of consciousness?
o
o
o
o
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A good way of ascertaining this is to ask if the patient remembers falling.
Syncope (or blackouts) can be associated with cardiac or neurological symptoms.
Was there any warning before the fall? If terms like 'giddy', 'dizzy' or 'faint' are used, explore
what is meant.
How long did it last?
Was there a seizure?
o
o
A witness can describe exactly what happened.
If tonic and clonic phases of convulsion - this does not necessarily imply epilepsy from a spaceoccupying lesion or cerebral degeneration, as cerebral ischaemia from poor CO e.g. due to
arrhythmia can produce the same.
After
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How was the patient after the fall?
Whilst they may have felt shaken or injured, features such as weakness that made getting up
again difficult, aching muscles or disorientation may indicate the postictal phase of a fit.
o A witness may be better at ascertaining confusion following the fall and noting how long it
lasted.
o The weakness of a transient ischaemic attack (TIA) may last just a few minutes and leave no
residue. Difficulty with language may indicate a TIA.
Injuries or incontinence?
o Incontinence is an unreliable sign of epilepsy and can occur with other causes of loss of
consciousness. A bitten tongue is more specific.
o Did any other injuries occur
Patients should be asked whether they were able to get back up without help after falling
o
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Review of systems
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Areas of pain or injury
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Chest pain / palpitations
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Previous syncopal events
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Bloody or tarry stool / heavy menses (anaemia)
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Vomiting / diarrhoea / excess urination (dehydration / electrolyte abnormalities)
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Is appetite good and weight steady? How is mobility? Is locomotion becoming slow and laboured?
Are mental faculties still sound or is there evidence of cognitive decline?
Past medical history
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Note history of heart disease and diabetes. Is the patient at increased risk of arrhythmias, TIAs,
stroke, peripheral neuropathies or hypoglycaemic episodes, for example?
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Know seizure disorder
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Risk factors for PE (recent surgery, immonilisation, cancer…)
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Brittle bone disease / osteoporosis (risk of fractures)
Drug history
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Review all drugs, especially those that may cause confusion or sedation.
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Most modern treatments for hypertension are less likely to produce postural hypotension than
older ones but it may still occur. Alpha-blockers, including phenothiazines can ↓ BP
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In general, the risk presented by benzodiazepine hypnotics outweighs benefit in the elderly.
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Ask about illicit and over the counter medications
FH - Family history should note presence at a young age of heart disease or sudden death in any
family member.
Social history
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What is the history of alcohol consumption? CAGE screening questionnaire
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Housing / accommodation
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What is the normal functional status of the patient? Do they require assistance dressing, washing,
cooking, for example?
 Targeted exam of CNS, CVS, MSS and vision.
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If the fall occurred recently, temperature should be measured to determine whether fever was a
factor.
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Inspection and assessment of any injuries sustained
 (e.g. bruising, swelling, tenderness, tongue bite)
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Mental state:
Does the patient seem alert and orientated or vague and confused?
Oriented to time, place and person? – orientation
Spell WORLD backwards – attention
Apple, ball, table word recall – immediate recall, short term memory
The mini mental state examination may be useful.
 Decline in mental state may indicate a cause for the falls or it may be the result if head injury
has caused a chronic subdural haematoma.
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Visual impairment:
Visual acuity / Snellen chart
Light reflexes
Colour vision test (perception of the colour red is 1st to go in pathology)
Accommodation
- Visual fields
- Eye movements / nystagmus
 Abnormalities in visual acuity should trigger a more detailed visual examination by an
optometrist or ophthalmologist.
 Macular degeneration and visual field defects may predispose to falls.
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Cardiovascular examination:
AF? Variable heart block? Bradycardia? Tachycardia may be a feature of congestive heart
failure
Lying and standing BP: After 1 and then 5 minutes of standing. *A drop of more than 20 mm
Hg in the systolic blood pressure on standing is significant*
Listen for bruits over the bifurcation of the carotid arteries but also in the posterior triangle of
the neck to detect bruits from the vertebral arteries.
If any murmurs: note any change with a Valsalva maneuver, standing, or squatting is noted.
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Neurological
Note muscle wasting that may reflect disuse atrophy, often secondary to arthritis.
Brief assessment of the sensory system - ? peripheral neuropathy. Loss of vibration sense can
be a marker for posterior column disease with associated loss of proprioception.
Basic postural control and the proprioceptive and vestibular systems are evaluated using the
Romberg test (in which patients stand with feet together and eyes closed).
Tests to establish high-level balance function include the one-legged stance and tandem gait.
If patients can stand on one leg for 10 sec with their eyes open and have an accurate 3-m (10ft) tandem gait, any intrinsic postural control deficit is likely to be minimal.
Try to reproduce vertebrobasilar symptoms by asking the patient to extend their neck to the
full and to hold it for several seconds and repeat with flexion and full rotation to left and right.
Evaluate positional vestibular function (e.g. with the Dix-Hallpike maneuver*)
Check coordination (including cerebellar function + nystagmus), stationary balance, and gait.
* The Dix–Hallpike test
o Is performed with the patient sitting upright with the legs extended.
o The patient's head is then rotated by approximately 45 degrees.
o The clinician helps the patient to lie down backwards quickly with the
head held in approximately 20 degrees of extension. This extension may
be achieved by having the clinician supporting the head as it hangs off
the table or by placing a pillow under their upper back.
o The patient's eyes are then observed for about 45 seconds as there is a characteristic 5-10 second
period of latency prior to the onset of nystagmus.
o If rotational nystagmus occurs then the test is considered positive for benign positional vertigo.
o During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the
ear closest to the ground. The direction of the fast phase is defined by the rotation of the top of the eye,
either clockwise or counter-clockwise.
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Musculo-skeletal:
The neck, spine, and extremities (especially the legs and feet) should be evaluated for
weakness, deformities, pain, and limitation in range of motion.
Note how the patient gets up from the chair. There may be proximal myopathy but in the
elderly disuse atrophy is more common. Is gait normal? Is there asymmetry? Some gait
abnormalities may be due to arthritis. Look for features that may indicate Parkinson's disease.
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Performance test
NICE recommends the following as being pragmatic tests:
- Timed Up & Go Test: Observe for unsteadiness as the patient rises from their chair without
using their arms, walks 10 feet, turns around, walks back and resumes a sitting position. A
walking aid can be used if required. The process should take less than 16 seconds. Patients
who have difficulties are at an increased risk of falling and need fuller evaluation.
- Turn 180° Test: request that the patient stand up and step around until they are facing the
opposite direction. If more than four steps are required to do this, further assessment is
indicated.
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Abdominal examination
Abdomen is palpated for tenderness / ascities
A rectal examination is done to check for gross or occult blood.
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Red flags: Certain findings raise suspicion of a more serious aetiology of syncope:
Syncope during exertion
Multiple recurrences within a short time
Heart murmur or other findings suggesting structural heart disease (eg, chest pain)
Older age
Significant injury during syncope
Family history of sudden unexpected death
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Investigations
Basic blood tests including:
o FBC (macrocytosis may indicate alcohol abuse / anaemia)
o Hct is measured if anemia is suspected.
o U+E (dehydration, deranged electrolytes)
o LFTs (may indicate alcohol abuse, especially gamma GT)
o TFTs
o Vitamin B12
o Random blood glucose (DM – hypo or hyperglycaemia)
o Cardiac markers e.g. serum troponin, CK-MB (measured if acute MI is suspected)
o hCG - all females of childbearing age should have a pregnancy test.
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Urinalysis may reveal unsuspected DM (vascular disease, neuropathy, poor vision)
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Pulse oximetry (hypoxaemia - PE)
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If hypoxic, do CXR / CT to investigate PE
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ECG to confirm or suggest (+/- ambulatory ECG):
o Arrhythmia e.g. AF
o Conduction defects where there is a prolonged PR interval, inferior ischaemia or bundle
branch block
o Ventricular hypertrophy
o Pre-excitation
o QT prolongation
o Pacemaker malfunction
o Myocardial ischemia, or MI
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Echocardiography is indicated for patients with known: heart failure, atrial fibrillation and valvular
disease to assess ventricular or valvular function or to detect atrial thrombus OR with exerciseinduced syncope, cardiac murmurs, or suspected intracardiac tumors (e.g. those with positional
syncope).
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Tilt table testing is done if history and physical examination indicate vasodepressor or other reflexinduced syncope.
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Stress testing (exercise or pharmacologic) is done when intermittent myocardial ischemia is
suspected. It is often done for patients with exercise-induced symptoms.
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EEG is warranted if a seizure disorder is suspected.
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Visual assessment by an optician
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Spinal x-rays and cranial CT or MRI are indicated only when the history and physical examination
detect new neurologic abnormalities.
Patients with suspected arrhythmia, myocarditis, or ischemia should be evaluated as inpatients.
 If there are no clinical clues, measuring cardiac markers and obtaining serial ECGs to rule out MI
in older patients plus ECG monitoring for at least 24 h are prudent.
 Any detected arrhythmia must be associated with altered consciousness in order to be
implicated as the cause, but most patients do not experience syncope during monitoring.
 Effects of falls (e.g. fractures)
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Death
Falls are the 6th leading cause of death
Some fall-related injuries are fatal.
Up to ¼ of frequent fallers die within 1 year of presentation due to underlying cause of falls
If neck of femur is #, mortality is: 10% in 1 month, 30% in 1 year (due to immobility, frailty, perioperative complications)
Physical injury
Over 50% of falls among elderly people result in an injury.
Although most injuries are not serious (e.g. contusions, abrasions), fall-related injuries account for
about 5% of hospitalizations in patients ≥ 65.
Other serious injuries (e.g. head and internal injuries, lacerations) occur in about 10% of falls.
More common/severe if lack of protective subcutaneous fat
Fractures (#)
About 5% of falls result in fractures of the humerus, wrist (including Colles' fracture and
dislocations of the wrist), or pelvis. About 2% of falls result in a hip fracture.
Fractures of the femur
If >80 years old 10% fracture their hips when they fall
Fractured hips are a major cause of loss of independence and morbidity and even mortality.
Risk increases with:
o Osteoporosis
o Osteomalacia
o Paget's disease of bone
o Metastases (to bone)
Sequale of a long lie: remaining on the floor for >1 hour after falling
Pressure sores
Hypothermia
Hypostatic pneumonia
50% die within 6 months of the fall, even if there was no injury sustained
Renal failure via: 1) Dehydration 2) Muscle breakdown – causes release of creatinine kinase –
causing rhabdomyelitis
Psychological injury
- Loss of self-confidence and independence
- Fear of falling (commonest fear in older people)
- Decreased activity - Some people may even avoid certain activities (eg, shopping, cleaning)
because of this fear. (Decreased activity can increase joint stiffness and weakness, further
reducing mobility.)
- Physical dependence
- Increased medication use
- Decreased quality of life
- Anxiety and depression
- Acceptance / expectation of falls in older age
 Aware of factors determining good outcomes
 Understand prevention of falls
 Muscle strengthening and balance retraining – e.g. physiotherapy.
 A wide variety of activities (from dancing to Tai Chi) can be undertaken often with the secondary
gain of social contact. Activity also slows osteoporosis and helps to prevent weight gain which
further impairs mobility.
 Home hazard modification
 Withdrawal of psychotropic medication
 Pacing for those with carotid sinus hypersensitivity
 Hip protectors - there is no good evidence for the efficacy of hip protectors in preventing fractures
in older people who fall whilst living independently. They may be effective in those living in
institutional care who are at high risk of hip fracture but acceptance and adherence is poor as they
are uncomfortable and difficult to get on and off quickly.
 NICE recommends that all people at risk of falls should be offered a home assessment and
interventions to modify environmental hazards e.g.:
- Loose rugs or mats (especially on a slippery floor)
- Lighting
- Electric leads (trailing across the floor)
- Wet surfaces (especially bathroom)
- Stairs (indoor/outdoor)
 Referral to an optician can be useful in diagnosis and management.
 Give advice on appropriate footwear
 Education on how to fall safely, and how to rise from the floor without help
 Install personal alarm systems
 Other interventions (e.g. nutritional supplementation, cognitive behavioural therapy) - efficacy is
unknown
Fragility (osteoporosis)
 Ca2+ / Vitamin D
 Bisphosphonates (hip+vertebral #
within 6 months)
Fracture
prevention
triangle
Falls
 MDT e.g. phsyio, OT,
medical review,
education, exercise,
 confidence
Force
 Learning ‘how to fall’
 Hip protectors
 Psychopathology of ageing.
Geriatric giants:
1)
2)
3)
4)
Immobility
Incontinence
Impaired intellect
Instability
Psychopathology
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Increased depression and anxiety
Dementia
Delirium
Psychological injury of falls
General effects of aging re: increased risk of falls
- Body sway increases ( Females > Males)
- Reaction time slows
- Reflexes may be decreased
- Walking patterns become more irregular
- Visual impairment more common
- Decreased proprioception in toes/feet
- Decreased confidence
Co-morbidities
Mechanisms of cellular senescence and somatic
ageing
• Generation of free radicals
– Failure of oxygen scavenging in cells
– Environmentally-induced free radicals
• Cumulative defects in DNA integrity
• Glycation of proteins
• Telomeric shortening
 Correctly categorises cause of fall/collapse.
Causes of falls in older people are usually multifactorial but include:
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Accident and environmental hazards (31%)
Gait and balance disorders or weakness (17%)
Dizziness and vertigo (13%)
Drop attack* (9%)
Confusion (5%)
Postural hypotension (3%)
Visual disorder (2%)
Syncope (0.3%)
Other specified causes including arthritis, acute illness, drugs, alcohol*, pain, epilepsy and
falling from bed (15%)
Unknown (5%)
Do not forget the possibility of elder abuse.
*Drop attacks
Drop attacks refer to a fall in which the cause is unknown, the event unexpected and there is no
loss of consciousness. Not a term used very often in modern medicine, as it is not a diagnosis.
*Alcohol
 Intoxication causes acute instability.
 Chronic alcoholism may cause complications predisposing to falls:
- Polyneuropathy
- Wernicke's encephalopathy
- Korsakoff's syndrome
Neurological problems
 TIAs / strokes can cause significant weakness.
 Parkinson's disease impairs mobility (abnormal posture, freezing of gait, frontal impairment,
poor leaning balance and leg weakness are independent risk factors). 10
 Diabetes related neuropathy
 Proximal myopathy (from, for example, thyrotoxicosis, Cushing's syndrome and use of
steroids) may impair mobility, particularly rising from sitting.
 Cognitive impairment may impair co-ordination.
 Instability (musculoskeletal and neuromuscular causes)
Mechanism of fall
Gait
Example conditions
Arthritis
Foot deformities
Muscle weakness
Proprioception
Peripheral neuropathy (eg, due to diabetes mellitus)
Vitamin B12 deficiency
Otolaryngologic
function
Acute labyrinthitis
Benign paroxysmal positional vertigo
Hearing loss
Meniere's disease
Postural and
Cerebellar degeneration
neuromotor function Myelopathy (eg, due to cervical or lumbar spondylosis)
Parkinson's disease
Peripheral neuropathy
Stroke
Vertebrobasilar insufficiency
Causes of immobility / instability
in joints
Osteoarthritis
Rheumatoid arthritis
Pseudogout
Infection
Neuronal damage
Hemiplegia
Peripheral neuropathy
Motor neurone disease
Paraplegia
Fear and anxiety
Manipulative behaviour
Depression
Dementia
Pain/stiffness
In muscles
Myositis
Polymyalgia rheumatic
Parkinson’s disease
Weakness
Muscle damage
Disuse
Myopahty
Amyotrophy
Hypokalaemia
In bones
Osteoporosis
Osteomalacia
Malignancy metastases
Reduced effort tolerance
Dyspnoea
Anaemia
Decreased cardiac output
Psychological causes
Re: falling
Attention seeking
Apathy and decreased initiative
Decreased insight into need to maintain mobility
 Understand heart rhythm.
 Able to interpret common ECG abnormalities that may lead to sycope.
 Able to initiate emergency care for life threatening arrhythmia.
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In witnessed syncope, pulses are checked immediately.
If the patient is pulseless, CPR is begun and cardiac resuscitation is done.
If pulses are present treat according to the arrhythmia
Placing the patient in a horizontal position with legs elevated typically ends the syncopal episode if
life-threatening disorders are ruled out.
Reference: a normal ECG rhythm strip
When looking at an ECG, comment on:
 Rate – under 60bpm is slow, over 100bpm is fast
 Regularity – look at R-R distances. Are they regular/ occasionally irregular/
regularly irregular/ irregularly irregular
 P waves – are they present, do they look alike, do they occur at a regular
rate, is there one before each QRS
 PR interval – normal is 0.12-0.20 ms (3-5 small boxes)
 QRS duration – normal is 0.04 – 0.12 ms (1-3 small boxes)
Sinus arrhymias = sinus rhythm is present (i.e. P wave precedes every QRS) but rate is ↓/↑
1) Sinus bradycardia – < 60bpm
2) Sinus tachycardia – > 100bpm
Causes: Physiological in resting athletes, drugs,
sick sinus syndrome, hyopthyroidism
Causes: Physiological in exercise/ stress
ECG:
ECG:
 Rate less than 60bpm
 Regular rhythm
 P waves present
PR interval and QRS duration normal
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Rate over 100bpm
Regular rhythm
P waves present
PR interval and QRS duration normal
Management: stop/treat causative factors, give
atropine. External transthoracic pacing can be
used - Isoproterenol can be used to maintain
adequate heart rate while a temporary
pacemaker is placed.
Management: A direct-current synchronized
shock is quicker and safer for unstable patients.
Inadequate venous return is treated by keeping
the patient supine, raising the legs, and giving IV
normal saline.
Premature ventricular contractions/ ventricular ectopic beats
Ventricular ectopics in isolation are not a problem – but can be dangerous if they occur one after the
other. Usually benign in younger patients, more serious in the elderly. Exercise can increase or decrease
frequency in different patients
Causes:
× Exercise/ post-exercise
× Hormonal changes in females
× Ischaemic heart disease
× Bundle-branch block
× Digoxin toxicity
× Reperfusion therapy after MI
× Electrolyte changes
×
×
×
×
×
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Increased catecholamines
Hypoxia/hypercapnia
Illicit substances
Mitral valve prolapsed
Cardiomyopathy
Myocarditis
Features: ● Usually asymptomatic ● Palpitations: ‘Heart misses a beat’ / ‘Heart jumps/flutters’ ● Neck or
chest discomfort ● Syncope
ECG:
 Aside from ectopic, sinus rhythm
 Broad QRS complex in ectopic beat– over 0.12 seconds
 Downward deflection of QRS complex occurs as the depolarisation comes from the ventricles at
the back of the heart
Treatment: Beta-blocker if symptomatic
AV nodal blocks
1) 1st degree AV block - benign
Causes: Beta-blockers
ECG:
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Rate – may be slow
Regular rhythm
P waves normal
PR interval prolonged (>0.20 sec)
QRS duration normal
2) 2nd degree AV block, Mobitz type I (Wenckebach) – usually benign
ECG:
 Rate – slow
 Regularly irregular rhythm
 P waves are present, although some
have no QRS
 With each successive QRS the P-R
interval ↑ until there is a nonconducted p wave
 QRS duration normal
3) 2nd degree AV block, Mobitz type II – may require a pacemaker
ECG:
 Rate – slow
 Regular rhythm
 P waves are present, but some not
have a QRS complex – if QRS is
missed it will be a 2:1 or 3:1 block
 PR interval normal or prolonged
 QRS normal
Management: May need a pacemaker
4) 3rd degree AV block
 Rate – bradycardic
 Rhythm – 2 independent rhythms are on
the ECG:
 The P waves with a regular P-P interval
represent the first rhythm.
 The QRS complexes with a regular R-R
interval represent the second rhythm.
 P-R interval is variable as there is no coordination between P waves & QRS complexes.
 QRS broad, over 0.12 seconds.
 May see downward deflection of QRS as ventricles generate their own rhythm
Management: requires a pacemaker as no correlation between P waves and QRS complexes
Supraventricular arrhythmias
1) Paroxysmal supraventricular (narrow complex) tachycardia
Causes: Common in young women. Structural defects may predispose
Features:
 Palpitations: heart racing or fluttering
 Lightheadedness
 Polyuria
ECG:
ECG shows a paroxysm of narrow complex tachycardia occurring
 Rate – tachycardic
 Rhythm – changes from sinus rhythm to a regular tachycardia
 P waves not present in paroxysm
 PR interval normal
 narrow QRS complex during paroxysm – less than 0.04
Management: vagotonic manoeuvres, followed by adenosine or verapamil (if not on Beta-blockers). LT
maintenance: beta-blockers / verapamil
Ventricular arrhythmias – both are a medical emergency
1) Ventricular tachycardia
Causes: If pulse present…
× Hyperkalaemia
× MI
× Ischaemic heart disease
Features:
 Palpitations: heart racing or
fluttering
 Breathlessness
 Syncope
 May or may not have a pulse
ECG:
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Rate – over 150bpm
Regular rhythm
No P waves
Broad QRS complex – over 0.12 seconds
Downwards deflection of QRS
Management: Amiodarone or lidocaine. Cardioversion if haemodynamically unstable.
2) Ventricular fibrillation
Features: No pulse – cardiac arrest
Management:
1) Defibrillate for 1st time
i) Defibrillation monophasic 360J OR
ii) Defibrillation biphasic 150–200 J (120J is acceptable, STHFT Defibs start at this)
2) Recommence CPR for 2 minutes, pause to check the monitor – if VF persists defibrillate for 2nd time,
as above.
3) Resume CPR for 2 minutes – check monitor. If still VF – Deliver 3rd shock.
4) I.V. administration of Adrenaline 1mg and Amioderone 300mg.
 Able to perform ECG (See clinical skills info on Minerva)
Limb leads use mnemonic "Ride
Your Green Bike"(clockwise):




Ride - Red - right arm
Your - Yellow - left arm
Green - Green - left leg
Bike - Black - right leg
 Performs appropriate tests for postural hypotension
o Record blood pressure sitting.
o Record after 1 minute of standing.
o Record afte 5 minutes of standing.
*A drop of more than 20 mm Hg in the systolic blood pressure on standing is significant*
 Able to explain 24 hour cardiac monitoring
Holter monitor (24h): A Holter monitor is a machine that continuously records the heart's
rhythms. The monitor is usually worn for 24 - 48 hours during normal activity.
How the Test is Performed
Electrodes (small conducting patches) are stuck onto your chest and attached to a small
recording monitor. You carry the Holter monitor in a pocket or small pouch worn around
your neck or waist. The monitor is battery operated.
While you wear the monitor, it records your heart's electrical activity. You should keep a
diary of what activities you do while wearing the monitor. After 24 - 48 hours, you return
the monitor to your doctor's office. The doctor will look at the records and see if there have
been any irregular heart rhythms.
How to Prepare for the Test
Tell your doctor if you are allergic to any tape or other adhesives. Make sure you shower or
bathe before you start the test - You will not be able to do so when wearing a Holter.
How the Test Will Feel
This is a painless test. Some people may need to have their chest shaved so the electrodes
can stick. You must keep the monitor close to your body. This may make sleeping difficult
for some people. You should continue your normal activities while wearing the monitor.
There are no risks associated with the test.
Why the Test is Performed
Holter monitoring is used to determine how the heart responds to normal activity:
 After a heart attack
 To diagnose heart rhythm problems
 When starting a new heart medicine
It may be used to diagnose:
 Atrial fibrillation/flutter
 Multifocal atrial tachycardia
 Palpitations
 Paroxysmal supraventricular tachycardia
 Reasons for fainting
 Slow heart rate (bradycardia)
 Ventricular tachycardia
Normal Results
Normal variations in heart rate occur with activities. A normal result is no significant
changes in heart rhythms or pattern.
What Abnormal Results Mean
Abnormal results may include various arrhythmias. Changes may mean that the heart is not
getting enough oxygen. The monitor may also detect conduction block, a condition in which
the atrial electrical activity is either delayed or does not continue into the ventricles of the
heart.
Considerations
Electrodes must be firmly attached to the chest so the machine gets an accurate recording
of the heart's activity.
While wearing the device, avoid:
 Electric blankets
 High-voltage areas
 Magnets
 Metal detectors
It is very important for you to keep a diary of symptoms. The diary should include the date,
time of day, type, and duration of symptoms.
 Control of upright posture.
Occularmotor
centre
Visual
Processed in
medulla
(pyramidal &
extrapyramidal)
Proprioception
Cerebellum
Spinal
cord
Vestibular
system
Muscle
Loss of proprioception in the feet is a common cause of ataxia. The ataxia markedly
improves simply by touching a stationary object or running the hand along the wall (in a
sense, replacing the lost sensitivity of the feet). Although elderly patients often lose some
sensitivity at the toes, the various causes of polyneuropathy or dorsal column damage
should be considered if the sensory loss is out of proportion for age.
The vestibular system contributes to balance and spatial orientation. The most common
disorders of the vestibular system are vesibular neuritis, a related condition – labyrinthitis,
and Benign Paroxysmal Positional Vertigo (BPPV).
The cerebellum contributes to coordination, precision and accurate timing of movements. It
receives input from sensory systems and from other parts of the brain and spinal cord, and
integrates these inputs to fine tune motor activity. Cerebeullum pathology causes disorders
in fine movement, equilibrium, posture, and motor learning.
Patients need adequate muscle strength to stay upright. Weakness due to myopahty,
neuropathy, or any UMN or LMN pathology can affect posture.
Extrapyramidal tracts are chiefly found in the reticular formation of the pons and
medullam, and are distinguished from the tracts of the motor cortex that reach their targets
by traveling through the "pyramids" of the medulla. Parkinson’s disease is an extrapyramidal
disorder which causes delayed postural corrections when the patient loses balance.
 Control of BP
Blood pressure = the pressure exerted by circulating blood upon the walls of blood vessels
The blood pressure is determined by the rate of blood flow produced by the heart (cardiac
output), and the resistance of the blood vessels to blood flow. This resistance is produced
mainly in the arterioles and is known as the systemic vascular resistance (SVR) or the
peripheral vascular resistance (PVR).
Blood pressure = cardiac output x SVR
Physiological mechanisms to maintain a normal BP are:
1) The autonomic nervous system is the most rapidly responding regulator of blood pressure
and receives continuous information from the baroreceptors (pressure sensitive nerve
endings) situated in the carotid sinus and the aortic arch. This information is relayed to the
brainstem to the vasomotor centre (VMC). A decrease in blood pressure causes activation of
the sympathetic nervous system resulting in increased contractility of the heart (beta
receptors) and vasoconstriction of both the arterial and venous side of the circulation (alpha
receptors).
2) The Capillary fluid shift mechanism refers to the exchange of fluid that occurs across the
capillary membrane between the blood and the interstitial fluid. This fluid movement is
controlled by the capillary blood pressure, the interstitial fluid pressure and the colloid
osmotic pressure of the plasma. Low blood pressure results in fluid moving from the
interstitial space into the circulation helping to restore blood volume and blood pressure.
3) Hormonal mechanisms exist both for lowering and raising blood pressure. They act in
various ways including vasoconstriction, vasodilation and alteration of blood volume. The
principal hormones raising blood pressure are:
(a) Adrenaline and noradrenaline secreted from the adrenal medulla in response to
sympathetic nervous system stimulation. They increase cardiac output and cause
vasoconstriction and act very rapidly.
(b) Renin and angiotensin production is increased in the kidney when stimulated by
hypotension. Angiotensin is converted in the lung to Angiotensin II, which is a potent
vasoconstrictor. In addition these hormones stimulate the production of aldosterone
from the adrenal cortex which decreases urinary fluid and electrolyte loss from the
body. This system is responsible for the long term maintenance of blood pressure but is
also activated very rapidly in the presence of hypotension.
4) The kidneys also regulate the blood pressure by increasing or decreasing the blood volume;
they are the most important organs for the long term control of blood pressure.
 Pathophysiology of heart and its conducting system.
 Basics of cardiac pacing.
 Permanent pacemakers are implantable devices designed to alter the cardiac rhythm during
pathologic states.
 They are usually placed in the anterior chest wall, and have one or two wire leads which enter the
subclavian vein, travel to the right side of the heart, and are implanted into the wall of the right atrium
and/or right ventricle.
 Newer biventricular pacemakers, used in advanced heart failure, also have a lead to the left ventricle
via the coronary sinus.
 Each lead may serve to either pace a specific chamber, sense the intrinsic electrical activity of a
specific chamber, or both.
 A system of codes has been developed to easily describe each possible combination:
1
2
3
4 (optional)
Chambers Paced
Chambers
Sensed
Response to Sensed
Stimulus
Rate Modulation?
O (none)
O
O
O (non rate-responsive)
A (atrium)
A
T (triggered)
R (rate-responsive)
V (ventricle)
V
I (inhibited)
D (both atrium
D
D (both triggered
and ventricle)
and inhibited)








A fifth position is sometimes used to specify the absence or location of multisite pacing (i.e.
biventricular pacing for patients with end-stage left heart failure).
The term triggered means that an output pulse is created in response to a sensed event,
whereas inhibited means that the output pulse is blocked in response to a sensed stimulus and
that the pacemaker then cycles for one or more timing cycles.
Pacemakers capable of rate modulation can increase their pacing rate in response to vibration,
minute ventilation, temperature, oxygen saturation, or other stimuli, independent of the heart’s
intrinsic activity.
Most modern pacemakers are capable of mode switching in response to sustained atrial
arrhythmias to prevent extreme ventricular response rates (i.e. DDD  VVI in the setting of atrial
flutter).
Understand pathology of index condition.
Mechanisms and effects of syncope
Cardiovascular causes of syncope (e.g. arrhythmias, aortic stenosis, vasovagal).
Postural hypotension (e.g. drugs, autonomic neuropathy).
Syncope is a sudden, brief loss of consciousness (LOC) with loss of postural tone followed by
spontaneous revival. The patient is motionless and limp and usually has cool extremities, a
weak pulse and shallow breathing.
Near syncope is light-headedness and a sense of an impending faint without LOC.
Fainting – a reflex:
• Afferent limb
– Various: Pain, emotion, smell, etc.
– Integration by deep brain centres
– Project to Medulla oblongata and centres in the floor of the fourth ventricle
especiallu nucleus of the Xth cranial nerve (Vagus) which become over active.
• Efferent limb Vagus
• Vagus causes sweating, fall in HR and venous pooling (especially splanchnic)
– Result very low CO
• Over flow of neural activity in brain to other regulatory centres especially emetic centre
– causing nausea
• Collapse
– CO insufficient for cerebral perfusion
• Restoration of consciousness (if allowed to become supine)
– Supine posture allows massive increase in VR (especially if legs put in air)
– Massive release of adrenaline causes rise in HR and increase in contractility
Normal CV reflexes on standing:
• Blood pools in limbs
• Baroreceptors sense fall in volume and pulse pressure and cause:
– Rise in HR
– Peripheral vasoconstriction (arteriolar and venous splanchnic and peripheral)
– Closure of pre capillary sphincters in limbs
CAUSES OF SYNCOPE
Most syncope results from insufficient cerebral blood flow. Some cases involve adequate
flow but insufficient substrate (O2, glucose or both) – in practice: hypoxia rarely develops
acutely to cause syncope (except in diving / plane accidents), and hypoglycaemia usually
gives warning symptoms (except in patients taking β-blockers).
Insufficient cerebral blood flow
5) Structural cardio-pulmonary conditions -  cardiac output
 Exercise, vasodilation and hypovolaemia exacerbate
 +/- chest pain, palpitations
 Occurs in any position (i.e. supine/standing)
 Onset and recovery is prompt
 Obstruction of outflow e.g. aortic / mitral stenosis, tetralogy of Fallot
 Systolic / diastolic dysfunction e.g. ischaemia + heart failure / hypertrophic
cardiomyopathy, restrictive myopathy, myocardial rupture, MI
 Cardiac tumours e.g. atrial myxoma
 Pericardial tamponade / constriction
 Pulmonary emobilism / pulmonary hypertension / amniotic fluid embolism / air
embolism
6) Arrhythmias
 Occurs in any position (i.e. supine/standing)
 Onset and recovery is prompt
 More common if patient taking drugs, especially antiarrhythmics
 More common if patient has structural heart disease; A systolic click followed by a
blowing systolic murmur that moves closer to the 1st heart sound on standing suggests
mitral valve prolapse (suggesting the cause is an arrhythmia).
Tachyarrhythmias: too fast to allow adequate ventricular filling (e.g. >150 – 180bpm)
Bradyarrhythmias: too slow to provide adequate output (e.g. <30 – 35bpm) – due to sick
sinus syndrome, high-grade atrioventricular block, drugs.
 Sinus node dysfunction (incl. brady/tachy)
 Atrioventricular conduction disorders
 Paroxysmal supraventricular and ventricular tachycardias
 Inherited syndromes (e.g. QT syndromes, Brugada syndrome)
 Induced by drugs/ implanted device malfunction (pacemaker, ICD)
7) Neurally-mediated reflex syncopal syndromes
 Warning symptoms e.g. dizziness, nausea, sweating
 Recovery prompt but not immediate (5-15 mins)
 Precipitant usually apparent






Vaso-vagal / situational faints do not occur in the supine position
Vaso-vagal faint
Strong emotion e.g. pain, fear, sight of blood
Situational faint
GI stimulation e.g. swallowing, defecation
Increased intrathroacic pressure e.g. tension pneumothorax / cough / sneeze /
straining to urinate or defecate / valsalva manoeuvre
Carotid sinus pressure/hypersensitivity (baroreceptors at the common carotid artery
bifurcation)
Glossopharyngeal and trigeminal neuralgial
Anaphylaxis
4) Orthostatic hypotension – failure of sinus tachycardia and/or vasoconstriction (autonomic
nervous system) to compensate for decrease in venous return on standing
 Symptoms develop within several minutes of assuming upright position
 Drop in BP with standing during examination
 Orthostatic syncope does not occur in the supine position
 Drugs and alcohol
 Autonomic dysfunction
 Anaemia
 Hypovolaemia
 Deconditioning due to long-term bed rest
 Addison’s disease (adrenal insuffiency)
 Micturition syncope
- Occurs in men. Plexus around the bladder is constricted if bladder full. When
bladder empties, the venous plexus fills via blood from legs, this decreases venous
return
5) Cerebrovascular – CVAs/TIAs rarely cause syncope because most of them do not involve the
centrencephalic structures that must be affected to produce LOC. Except, rarely:
 ‘Steal’ syndromes can cause syncope when a blood vessel has to supply both part of the
brain and an arm
 Basilar artery
 TIA/CVA
 Migraine
Other
 Pregnancy
 Prolonged standing
 Hyperventilation
 Hypoglycaemia
Features that suggest a non-syncopal attack
-
Confusion after attack for >5 minutes (seizure)
Prolonged (>15 seconds) tonic-clonic movements starting at the onset of the attack
(seizure)
Frequent attacks with somatic complaints, no organic heart disease, responsive or
partially responsive during attacks (psychiatric)
Associated with vertigo, dysarthria, diplopia (TIA)
 Postural hypotension (e.g. drugs, autonomic neuropathy).
Syncope that occurs most often when assuming an upright position (particularly in elderly
patients after prolonged bed rest or in patients taking drugs in certain classes) suggests
orthostatic syncope.
Syncope that occurs after standing for long periods without moving is usually due to venous
pooling.
Factors include rigid, noncompliant arteries, reduced skeletal muscle pumping of venous
return due to physical inactivity, and degeneration of the sinoatrial node and conduction
system due to progressive structural heart disease.
Some disorders that affect BP regulation:


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





Anemia
Arrhythmias
Cardioinhibitory carotid sinus hypersensitivity
COPD
Dehydration
Infections (eg, pneumonia, sepsis)
Metabolic disorders (eg, thyroid disorders, hypoglycemia, hyperglycemia with
hyperosmolar dehydration)
Neurocardiogenic inhibition after micturition
Postprandial hypotension
Valvular heart disorders
Some drugs that increase orthostatic hypotension:







Most antihypertensives (rarely β-blockers)
Antipsychotics (mainly phenothiazines)
Doxorubicin
Levodopa
Loop diuretics
Nitrates (with or without a phosphodiesterase inhibitor for erectile dysfunction)
Quinidine
Tricyclic antidepressants
Vincristine