Hypertension Flashcards
Is a single measurement of ↑ BP sufficient to diagnose Hypertension?
NO!!
What is the process for determing a patient’s BP in clinc?
- Measure BP in both arms
- If difference in BP is > 20 mmHg –> repeat measurements
- If difference remains > 20 mmHg on the 2nd measurement –> measure subsequent BPs in the arm with the higher BP
- If BP is measured as 140/90 or higher –> take 2nd measurement during consultation
- If 2nd measurement is substantially different from the 1st –> take a 3rd BP measurement
- Record the lower of the last 2 measurements (2nd or 3rd) as the BP
How do you confirm a diagnosis of HTN after a recorded clinic BP of 140/90 or higher?
- If clinic BP is 140/90 or higher –> offer ABPM (ambulatory blood pressure monitoring) to confirm diagnosis, ensure that:
- At least 2 measurements per hour - during ususal waking hours
- Use average of at least 14 measurements to confirm diagnosis
- If pt unabale to tolerate ABPM –> HBPM (home blood pressure monitoring), ensure that:
- For each BP recording, 2 consecutive measurements are taken, at least 1 minute apart and with the person seated
- BP is recorded twice/day (ideally in the morning and evening)
- BP recording continues for at least 4 days (ideally for 7 days)
- Discard measurements taken on the 1st day + use the average value of all the remaining measurements to confirm a diagnosis of HTN
What are the grades for severity of Hypertension?
- Isolated Systolic HTN = >140 / >90
-
Grade 1 (mild) = clinic BP 140-159 / 90-99
- and ABPM daytime average / HBPM average of > 135/85
-
Grade 2 (moderate) = clinic BP >/= 160
- and ABPM / HBPM average of >/= 150/95
- Grade 3 (severe) = >180 / >110
For what 2 reasons is staging the severity of HTN important?
Severity grade impacts:
- Risk stratification of patient
- Guides next step in management
When a patient’s hypertension is stage 3 (severe) it can result in hypertensive emergency - what is this also known as? What does it involve?
Also known as Malignant Hypertension it is severe hypertension (BP ≥ 180/110 mmHg) WITH target organ damage
- Very high BP - systolic >180 or diastolic >120
-
Aetiology:
- Vasocontrictors intiate abrupt ↑ systemic vascular resistance
- Results in –> endothelial injury, deposition of platelets/fibrin, ischaemia –> prompts further release of vasoactive substances
- Involves organ damage:
- Encephalopathy - ↑ BP in cerebral arteries causes cerebral oedema –> ↑ ICP –> neurological disturbances / change in conciousness
-
Symptoms / Signs:
- Eye signs (opthalmoscopy):
- Papilloedema (must be present for diagnosis to be made)
- Retinal bleeding
- Cotton wool spots
- Chest pain - crushing/pressure
- Extreme ↑ BP
- SoB
- Pulmonary oedema
- Numbness/weakness of face/limbs - changes in power/tone
- Blurred vision
- Change in GCS/mental status:
- Anxiety, confusion, ↓ concentration, fatigue, lethargy
- Signs of ↑ ICP:
- Headache
- Nausea + vomiting
- Seizure
- Eye signs (opthalmoscopy):
-
Epidemiology:
- M > F
- Affects 1% of those with HTN
-
Management:
- BP needs to be ↓ within a few minutes up to 2hrs using IV antihypertensives
- Labetalol (alpha and beta adrenergic antagonist) –> ↓ peripheral vascular resistance via vasodilation (in short term use) + ↓ HR (in long term use)
- Nicardipine (Ca2+ channel blocker) - more selective for cerebral and coronary vessels than other Ca2+ antagonists –> causes vasodilation, ↓ BP
Severe hypertension (BP ≥ 180/110 mmHg) WITHOUT target-organ damage is defined as what?
Hypertensive urgency (not emergency)
- BP needs to be ↓ gradually over 24-48 hrs with ORAL antihypertensives (as opposed to minutes-2hrs and IV in hypertensive emergency)
What factors affect Cardiac Output?
CO = HR x stroke volume
What factors affect blood pressure?
MAP (mean arterial blood pressure) = CO x PVR (peripheral vascular resistance)
Which 4 organs in the body are common sites of damage/modification as a result of high BP?
-
Eyes
- Retinopathy/maculopathy
-
Brain
- Strokes
- Microaneurysms
-
Heart
- Compensative/adaptive cardiomegaly
- Ischaemic heart disease
- CCF (followed by pulmonary HTN)
- Sudden death
-
Kidneys
- Hypertensive nephropathy (HTN causing kidney pathology)
- Nephron arteriosclerosis –> ischaemia –> kidney atrophy (small kidneys)
- Glomerular ischaemia due to renal artery stenosis caused by plaques or stiffening
- Glomerular HTN can result in glomerular damage –> causing blood and protein leakage into urine
What 4 signs on the retina can be produced by high BP (seen on Opthalmoscopy)?
-
Papilloedema - optic disc swelling
- Venous engorgement (often 1st sign)
- Blurring of optic disc margin
- Paton’s lines - concentric/radial lines cascading from optic disc
-
Flame Haemorrhage - intraretinal haemorrhage (looks like bruise)
- Feather/flame shape indicates bleed occurs at level of nerve fibre layers
-
Hard exudates - small white/yellowish lipid deposits with sharp margins, which form due to capillary leakage (i.e. ↑ retinal vascular permeability)
- Often appear; waxy / shiny / glistening
-
Cotton wool spots - white spots which represent swelling of retinal nerve fibres due to microinfarctions
- Usually near optic disc
What are the 2 causes of Primary Hyperaldosteronism?
What metabolic disturbance does it cause?
- Conn’s Syndrome = Unilateral Aldosterone producing adenoma (~30% of cases) –> adrenalectomy
- Bilateral adrenal hyperplasia (~70% of cases) –> spironolactone
High aldosterone –> ↓ K+ and ↓ H+ but ↑ Na+ and ↑ BP = Hypokalaemic Alkalosis
Features:
- Alkalosis
- Hypertension (↑ BP)
- Hypokalaemia
- Muscle weakness, hypotonia
- Palpitations
- Hypokalaemia induced nephrogenic DI: polyuria + polydipsia
- ECG:
- T-wave flattening or inversion
- Prolonged PR interval
- Apparent Long QT - it only appears to shown long QT, but due to fusion of the T+U waves it is actually the QU segement not QT being viewed
- ST depression
- U-waves
What is Addison’s Disease?
Addison’s Disease = autoimmune destruction of adrenal glands causing –> hypoadrenalism (↓ cortisol + ↓ aldosterone)
Causes of Primary Hypoadrenalism:
- 80% of primary hypoadrenalism = Addison’s Disease
- TB, metastases, meningococcal septicaemia, HIV, antiphospholipid syndrome
Treatment:
- Ongoing: hydrocortisone (glucocorticoid) + fludrocortisone (mineralocorticoid)
- Mineralocorticoid dose is impacted by mineralocorticoid activity of glucocorticoid given
- Adrenal Crisis: 50-100mg IV every 6 hours for 1-3 days
Features:
- Lethargy + weakness
- Anorexia
- Weight loss
- Hyperpigmentation (especially palmar creases)
- ↓ BP
- ‘Salt-craving’ due to hyponatraemia
- Nausea / vomiting
- Hyperkalaemia + acidosis
- Hypoglycaemia
- Vitiligo
How do you test for Addison’s Disease?
Short SynACTHen Test
- Administer tetracosactide (synacthen) 250 micrograms IV/IM
- Check blood cortisol at time 0 and +30 mins
- Cortisol at +30min should be > 600 nmol/L (in normal person)
- If cortisol < 600 nmol/L –> Addison’s Disease
What % of cases are essential/primary hypertension vs secondary hypertension?
- Essential/primary hypertension = 90-95%
- Cause unknown
- Secondary hypertension = 5-10%
- This is hypertension due to an underlying pathology