Older Persons Medicine Flashcards
Postural hypotension is a common condition affecting around half of the elderly population living in a residential institution. How might it present?
Dizziness
Syncope (severe cases)
Falls
Fractures
Blurred vision
Nausea
Confusion
Weakness
Sometimes precipitated ie. by a cough, defecation
May occur several minutes after standing up
More frequent with:
Meals
Exercise
A warm environment
How is postural hypotension diagnosed?
Tilt-table testing can be used to confirm postural hypotension. Tilt-table testing involves placing the patient on a table with a foot-support. The table is tilted upward and blood pressure and pulse is measured while symptoms are recorded in various positions.
Lying standing blood pressure:patient should be lying for at least 5 minutes, taking the first BP and then standing to measure in the first minute and at 3 minutes.
A fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure is significant
Causes of postural hypotension occur?
Neurogenic (autonomic failure):
Parkinsons Disease
Type 2 diabetes mellitus
Small cell lung carcinoma, monoclonal gammopathies, light chain disease, or amyloid
Non-neurogenic:
Drugs: antidepressants (TCAs), vasodillators, diuretics, negative inotropes, opiates, insulin
Dehydration
Sepsis or other states inducing vasodilation
Cardiac impairment (aortic stenosis, MI, CHF)
Chronic hypertension (loss of baroreceptor reflex)
Adrenal insufficiency (reduced intravascular volume)
How is postural hypotension managed?
Depends on cause
Ensure adequate hydration (blood volume)
In particular, evaluate polypharmacy
Reduce adverse outcomes from falls (e.g. fall alarm, soft flooring)
Behavioural changes (e.g. rising from sitting slowly, adequate hydration - avoiding high risk behaviours)
Compression stockings (reduce venous pooling)
In patients with enough cognition, counter-manoeuvres against postural hypotension can be taught (raising toes, raising legs, crossing legs)
Measures to expand blood volume include keeping the head of the bed elevated (reverse Trendelenburg). This increases plasma volume by decreasing overnight diuresis, with activation of the renin-angiotensin-aldosterone system
Pharmacotherapy:
Fludrocortisone (note: poor evidence base)
Midodrine (autonomic dysfunction)
What is the pathophysiology of postural hypotension?
Upon standing blood shifts from the chest to below the diaphragm
Fluid shift reduces venous return to the heart, and therefore ventricular filling and preload.
Cardiac output and therefore blood pressure are reduced.
The gravity-induced reduction in blood pressure is detected by baroreceptors in the aortic arch and carotid sinus.
Baroreceptors trigger baroreflexes, including vasoconstriction and compensatory tachycardia to restore BP.
Sympathetic outflow increases, vagal nerve activity decreases which decreases parasympathetic innervation to the heart.
The baroreceptors also send signals to the arterioles and venules in the circulatory system to increase total peripheral resistance.
Blood pressure increases.
In postural hypotension these mechanisms to maintain BP are impaired so there is a postural drop, because of one or more of:
- Failure of baroreflexes (autonomic failure)
- Volume depletion
- End-organ dysfunction
What factors may exacerbate postural hypotension?
Rising quickly after prolonged sitting or recumbency
Prolonged motionless standing
Time of day (early morning after nocturnal diuresis)
Dehydration
Physical exertion
Alcohol intake
Carbohydrate-heavy meals
Straining during micturition or defecation
Fever
What drugs may cause postural hypotension?
Diuretics
Alpha-adrenoceptor blockers for prostatic hypertrophy
Antihypertensive drugs,
Insulin, levodopa, and tricyclic antidepressants can also cause vasodilation and postural hypotension in predisposed patients
Why are the elderly more susceptible to postural hypotension?
- More prone to hypovolemia:
- Increase in natriuretic peptides
- Decrease in renin, angiotensin and aldosterone with age
- Impaired ability to retain water and sodium as well as diminished thirst response - Age related changes to CVS:
- Decreased baroreflex sensitivity with impaired alpha-1 adrenergic vasoconstriction and affected HR response
- Chronic HTN (further reduced baroreflexes and sensitivity and left ventricular failure compliance)
- Blunted response to the sympathetic nervous system recruitment in BP control - Health conditions
- Polypharmacy and medications that cause postural hypotension more commonly prescribed to the elderly ( furosemide and terazosin), use of multiple anti-HTN agents
- Higher prevalence of co-morbidities which cause autonomic dysfunction such as T2DM
- Deconditioning from lack of exercise leads to increased likelihood of experiencing severe symptoms from postural hypotension
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What are the overall aims of management of postural hypotension and how are they achieved?
1.To raise standing blood pressure without also raising supine blood pressure
2.To reduce orthostatic symptoms
3. To increase the time the patient can stand
4. To improve the ability of patients to perform activities of daily living
Achieved by targeting physiological mechanisms in order to:
1. Reducing venous pooling
2. Increasing blood volume
3. Increasing vasoconstriction
How does fludrocortisone work to treat postural hypotension? What are the contraindication and side effects, and how is it taken?
Fludrocortisone is a synthetic mineralocorticoid that expands plasma volume
This medication can be useful if non-pharmacological measures and cessation of exacerbating medications have proved unsuccessful. It has demonstrated good efficacy for patients whose plasma volume fails to adequately increase with salt and bolus fluids
Contraindicated in patients with failure, ascites and chronic renal failure.
Side effects may include supine HTN, severe hypokalemia,
Taken OD in morning starting at 100mcg
How does Midodrine work to treat postural hypotension? What are the contraindication and side effects, and how is it taken?
Midodrine is a vasopressor that is short-acting and can be useful in neurogenic postural hypotension.
It has a short duration of action and the literature suggests that it can be effective when used in conjunction with fludrocortisone. However, it is largely ineffective in patients with low plasma volume.
Caution in patients with severe HF, urinary retention and underlying HTN.
Midodrine has unique side effects including supine hypertension, scalp paraesthesia and pilomotor reactions, such as goosebumps.
Midodrine can be titrated for dosing up to three times daily, with a starting dose of 2.5mg.
Brief outline of the cardiac conduction system?
The electrical impulse travels through the heart via a specific conduction pathway. The sinoatrial node (SAN) acts as the initial pacemaker before the impulse spreads throughout the atria and towards the atrioventricular node (AVN).
The depolarisation wave travels through the heart’s septum via the Bundle of His and Purkinje fibres. These are organised into the left and right bundle branches.
The right bundle branch then depolarises the right ventricle and the left bundle branch depolarises the left ventricle simultaneously. The septum itself is depolarised by the left bundle branch, meaning the septum is depolarised from left to right.
What part of an ECG trace represents atrial depolarisation?
P wave
What part of an ECG trace represents conduction through the AVN and ventricles?
PR interval
What part of an ECG trace represents ventricular depolarisation?
QRS complex
What part of the ECG trace represents ventricular repolarisation?
T wave
How long is a normal PR interval?
0.12-0.20 seconds / 3-5 small squares
How long is a normal QRS complex?
Less than 0.12s / 3 small squares
How does Right Bundle branch block appear on ECG?
QRS > 120 ms (3 small squares)
RSR’ pattern in V1-V3
Wide, slurred S wave in lateral leads – I, aVL, V5-V6
(MaRoW)
How does Left Bundle Branch Block appear on ECG?
QRS duration > 120ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads – I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave > 60ms in leads V5-V6
(WilLiaM)
What type of bundle branch block is ALWAYS pathological and how does it appear?
LEFT bundle branch block
QRS duration > 120ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads – I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave > 60ms in leads V5-V6
What is seen here and what is the pathophysiology?
Right bundle branch block:
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation through the bundle of His occurs only via the left bundle branch.
The left branch still depolarises the septum as normal.
The left ventricular wall depolarises as normal.
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway.
What is seen here and what is this pathophysiology?
Left bundle branch block:
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation down the bundle of His occurs only via the right bundle branch.
The septum is abnormally depolarised from right to left.
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.
What do blockages of the left bundle branches cause on ECG?
Anterior fascicle block, which is much more common, causes left axis deviation.
Posterior fascicle block may cause right axis deviation.
Blockage of both causes LBBB (left bundle branch block)
What is seen here and what does it occur?
Left Axis Deviation = QRS axis less than -30°.
Leads I and aVL are positive; leads II and aVF are negative
Occurs in:
- Left anterior fascicular block
- Left bundle branch block
- Left ventricular hypertrophy
- Inferior MI
- Ventricular ectopy
- Paced rhythm
- Wolff-Parkinson White syndrome
What is seen here and what does it occur?
Right Axis Deviation = QRS axis greater than +90°
Leads II, III and aVF are POSITIVE;
Leads I and aVL are NEGATIVE
Occurs in:
- Left posterior fascicular block
- Lateral myocardial infarction
- Right ventricular hypertrophy
- Acute lung disease (e.g. Pulmonary Embolus)
- Chronic lung disease (e.g. COPD)
- Ventricular ectopy
- Hyperkalaemia
- Sodium-channel blocker toxicity
- WPW syndrome
- Normal in children or thin adults with a horizontally positioned heart
How does first degree AV block appear on ECG?
First-degree heart block involves a fixed prolonged PR interval (>200 ms).
How does second-degree AV (type 1) appear on ECG?
Second-degree AV block (type 1) is also known as Mobitz type 1 AV block or Wenckebach phenomenon.
Typical ECG findings in Mobitz type 1 AV block include progressive prolongation of the PR interval until eventually the atrial impulse is not conducted and the QRS complex is dropped.
AV nodal conduction resumes with the next beat and the sequence of progressive PR interval prolongation and the eventual dropping of a QRS complex repeats itself.
How does second-degree AV (type 2) appear on ECG?
Second-degree AV block (type 2) is also known as Mobitz type 2 AV block.
Typical ECG findings in Mobitz type 2 AV block include a consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.
The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave.
How does Third-degree heart block (complete heart block) appear on ECG?
Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.
Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.
Cardiac function is maintained by a junctional or ventricular pacemaker.
Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His.
Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His.
Where do the various AV blocks occur?
First-degree AV block:
Occurs between the SA node and the AV node (i.e. within the atrium).
Second-degree AV block:
Mobitz I AV block (Wenckebach) occurs IN the AV node (this is the only piece of conductive tissue in the heart which exhibits the ability to conduct at different speeds).
Mobitz II AV block occurs AFTER the AV node in the bundle of His or Purkinje fibres.
Third-degree AV block:
Occurs at or after the AV node resulting in a complete blockade of distal conduction.
What might a shortened PR intevral suggest?
If the PR interval is shortened, this can mean one of two things:
Simply, the P wave is originating from somewhere closer to the AV node so the conduction takes less time (the SA node is not in a fixed place and some people’s atria are smaller than others).
The atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. This is an accessory pathway and can be associated with a delta wave (see below which demonstrates an ECG of a patient with Wolff Parkinson White syndrome).
When might a narrow QRS complex occur (< 0.12 seconds)
A narrow QRS complex occurs when the impulse is conducted down the bundle of His and the Purkinje fibre to the ventricles. This results in well organised synchronised ventricular depolarisation.
When might a broad QRS complex occur?
A broad QRS complex occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle. In contrast, an atrial ectopic would result in a narrow QRS complex because it would conduct down the normal conduction system of the heart. Similarly, a bundle branch block results in a broad QRS complex because the impulse gets to one ventricle rapidly down the intrinsic conduction system then has to spread slowly across the myocardium to the other ventricle.
What might a tall QRS on ECG suggest?
Tall complexes imply ventricular hypertrophy (although can be due to body habitus e.g. tall slim people).
What is a pathological Q wave?
A pathological Q wave is > 25% the size of the R wave that follows it or > 2mm in height and > 40ms in width.
May suggest MI
RVH features on ECG?
Diagnostic criteria
Right axis deviation of +110° or more.
Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
QRS duration < 120ms (i.e. changes not due to RBBB).
Supporting criteria
Right atrial enlargement (P pulmonale).
Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III.
Deep S waves in the lateral leads (I, aVL, V5-V6).
Other abnormalities caused by RVH:
Right bundle branch block (complete or incomplete).
LVH on ECG?
Voltage Criteria
Limb Leads
R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
S wave in aVR > 14 mm
Precordial Leads
R wave in V4, V5 or V6 > 26 mm
R wave in V5 or V6 plus S wave in V1 > 35 mm
Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria
Increased R wave peak time > 50 ms in leads V5 or V6
ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
Causes of LVH
Hypertension (most common cause)
Aortic stenosis
Aortic regurgitation
Mitral regurgitation
Coarctation of the aorta
Hypertrophic cardiomyopathy
Causes of RVH
Pulmonary hypertension
Mitral stenosis
Pulmonary embolism
Chronic lung disease (cor pulmonale)
Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis)
Arrhythmogenic right ventricular cardiomyopathy
What is AMTS?
Abbreviated Mental Test Score (AMTS)
It is a useful tool for determining the presence of cognitive impairment in a patient
Initially developed to pick up the presence of dementia, now commonly used to identify any confusion (acute or chronic)
What are the questions a patient is asked in AMTs?
One point awarded for each:
- Age
- Current time (to the nearest hour)
- Recall: Ask the patient to remember an address (e.g. 42 West Register Street)
- Ensure they are able to say it back to you immediately, then check recall at the end of the test
- Current year
- Current location (e.g. name of hospital or town)
- Recognise two people (e.g. relatives, carers, or if none around, the likely profession of easily identified people such as doctor/nurse)
- Date of birth
- Years of the first (or second) world war
- Name of the current monarch (or prime minister)
- Count sequentially backwards from 20 to 1
A score of less than 8 in the AMTS implies the presence of cognitive impairment
What are the limitations of the AMTS?
In a patient with reduced GCS (or language barrier) the test cannot be completed
The test was validated during the 1970s in the elderly population
As such, the first world war was a significant life event, that one would expect any elderly patient to recall but this may not be the case for younger patients
It does remain a useful initial screening tool, with high sensitivity, to identify elderly patients with cognitive impairment (e.g. delirium or dementia)
What are the advantages of the MMSE?
- Relatively quick and easy to perform
- Requires no additional equipment
- Can provide a method of monitoring deterioration over time
What are the disadvantages of the MMSE?
- Biased against people with poor education due to elements of language and mathematical testing
- Bias against visually impaired
- Limited examination of visuospatial cognitive ability
- Poor sensitivity at detected mild/early dementia
- Copyrighted and should the most up to date version should only be accessed via the Psychological Assessment Resourcing (PAR)
What is the MMSE?
Mini Mental State Examination is a 30-point test.
Screening tool used as a measure of cognitive impairment
Any score of 24 or more (out of 30) indicates a normal cognition.
Below this, scores can indicate severe (≤9 points), moderate (10–18 points) or mild (19–23 points) cognitive impairment.
The raw score may also need to be corrected for educational attainment and age.
What are some examples of healthcare aquired infections?
Bacteraemia
Gram-negative bacteria
Clostridioides difficile infection
Escherichia coli
Pseudomonas aeruginosa
Klebsiella species (Note that there is a rising incidence of carbapenem-resistant Enterobacteriaceae (CRE) and carbapenem-resistant Klebsiella)
Staphylococcus aureus (meticillin resistant Staphylococcus aureus or MRSA and meticillin sensitive Staphylococcus aureus or MSSA)
Surgical site infection
VRE
CRO
What is MRSA and how might it be managed?
Problem gram positive organisms
Staphylococcus aureus (S. aureus) is a common gram-positive bacterium that colonises human skin and mucous membranes
MRSA is Methicillin resistant staphylococcus aureus
Resistant to flucloxacillin. Usually acquired during exposure to hospitals and other healthcare facilities and can cause serious healthcare associated infections.
Vancomycin and teicoplanin (glycopeptide abx, narrow spectrum, covering most gram positives) may be used to manage MRSA infection. The are only available IV and cannot penetrate the blood-brain barrier as they are large molecules. Vancomycin is nephrotoxic so levels need to be measured.
Skin cleansers are used in combination with nasal ointment for MRSA skin decolonization; chlorhexidine 4% skin cleanser is the most common
Most commonly, intravenous teicoplanin is used for surgical prophylaxis in MRSA colonized patients undergoing surgical procedures
What is VRE and how is it managed?
Vancomycin-resistant enterococci (most also resistant to amoxicillin), including E. faecalis and E. faecium
Normal flora of the gut, but often colonise diabetic ulcers and sacral sores, as well as causing infections in immunocompromised patients (particularly meningitis, septicaemia, wound infections and endocarditis).
It is treated with oxazolidinones e.g. linezolid. Linezolid is a narrow spectrum gram-positive agent with excellent penetration into skin and brain. However, can cause bone marrow suppression, peripheral neuropathy, and optic neuritis.
What is a stage 1 pressure ulcer?
Stage 1 pressure injuries are characterized by superficial reddening of the skin (or red, blue or purple hues in darkly pigmented skin) that when pressed does not turn white ( non-blanchable erythema )
A stage 1 pressure ulcer affects only the epidermis, which is the upper layer of the skin. At this stage, the skin typically remains unbroken
Affected area may be painful, warm, firm
Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
What is a stage 2 pressure ulcer?
Stage 2 pressure ulcers are characterized by partial-thickness skin loss into but no deeper than the dermis. This includes intact or ruptured blisters.
Affected area is shiny and dry, there is no sloughing and no bruising
Shallow or open area
Wound bed is pink and red
Partial thickness skin loss involving epidermis or dermis, or both. The
ulcer is superficial and presents clinically as an abrasion or blister
What is a stage 3 pressure ulcer?
Stage 3 pressure ulcers involve full-thickness skin loss potentially extending into the subcutaneous tissue layer.
Shiny or dry
Shallow or open area
Wound bed is pink and red
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
What is a stage 4 pressure ulcer?
Stage 4 pressure ulcers extend deepely, exposing underlying muscle, tendon, cartilage or bone.
Slough or eschar may be present
Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss
What stage pressure ulcer is this?
Stage 4
What stage pressure ulcer is this?
Stage 3
What stage pressure ulcer is this?
Stage 1
What stage pressure ulcer is this?
Stage 2
What is a deep tissue injury?
Skin intact or blood filled blister
Localised area purple or maroon in colour
Underlying tissue may be affected
Painful, firm, boggy, warmer area of skin
These represent a serious form of pressure injury in that they form in the underlying tissues and are often not visible until they have advanced to the point where treatment is significantly more problematic. Deep tissue injuries are also known to deteriorate quickly even under optimal care.
What is this?
Deep tissue injury
What is an unstageable pressure ulcer?
Ulcers covered with slough or eschar are by definition unstageable. The base of the ulcer needs to be visible in order to properly stage the ulcer, though, as slough and eschar do not form on stage 1 pressure injuries or 2 pressure ulcers, the ulcer will reveal either a stage 3 or stage 4 pressure ulcer.
Full thickness tissue loss
What stage pressure ulcer is this?
Unstageable as slough and eschar covers the ulcer base, full depth of the ulcer cannot be established
Where might pressure ulcers occur?
Sacram
Buttocks
Ears
Back of head
Elbows
Heels
Shoulders
Trochanters
Spine
Knees
Toes
Malleolus
What do the numerical values of the clinical frailty score indicate?
1 Very fit
2 Well
3 Managing well (not active beyond routine walking)
4 Vulnerable (not dependent on other but symptoms limit activities)
5 Mildly frail (need help in high order IADLs)
6 Moderately frail (requiring help with all outside activities, minimal assistance with ADLs)
7 Severely frail - dependent on others for personal care
8 Very severely frail - completely dependent on othersm approaching end of life)
9 Terminally Ill (<6 months life expectancy)
