Cardiology JC010: High Blood Pressure: Hypertension Flashcards
Hypertension
- Persistently abnormally ↑ BP (>140/90)
- Progressive “CV syndrome” associated with target organs damage (often present before high BP values are observed, ∵ often asymptomatic)
- ↑ Systolic BP + Diastolic BP (equally important)
—> Risk: ↑ Diastolic > ↑ Systolic
—> ↑ 20 mmHg Systolic = ↑ 10 mmHg Diastolic
—> CV mortality risk ***doubles for every 20/10 mmHg increase
Isolated Systolic HT (ISH):
- ↑ Systolic BP without significant ↑ Diastolic
- common in elderly (∵ vascular stiffness —> lower diastolic)
Systolic BP:
血谷出去 (撐開血管的壓力)
Diastolic BP:
血管收縮 (反彈返去的壓力) / Resting pressure
Burden of hypertension
- 1 Billion people worldwide
- Deadliest preventable risk factor worldwide
- 2/3 in developing countries
- 1/3 in South East Asia adult
- 1.5 million people die of HT related diseases each year in SEA
Consequences of HT
- ↑ Stroke risk
- ↑ Coronary artery disease risk (e.g. MI)
DBP: 90 (relative risk = 1, ∴ used as cutoff)
***Uncontrolled HT and Risk for CVS events
記5樣: 腦, 眼, 心, 腎, 血管
High risk for:
- Cardiac
- Cerebral
- Renal
HT
—> Asymptomatic organ damage —>
1. LV hypertrophy
2. Hypertensive retinopathy
3. Hypertensive nephrosclerosis
4. Other vascular damage
—> Symptomatic organ damage —>
1. HF
2. Cerebrovascular disease
3. Kidney failure
4. CAD
5. Peripheral vascular disease
—> Death
What cause “essential” HT?
Essential HT = Primary HT (vs Secondary HT)
No single risk factor for HT (for 90-95%)
1. Environmental
2. Genetic
Mechanisms of HT
Young subjects:
- ↑ Adrenergic drive in CNS (e.g. lot of stress) —> **↑ CO, **↑ PVR
- ***↑ RAAS activation in Kidney
Elderly subjects:
- ↑ PVR (∵ degeneration)
Solution:
- Block Sympathetic tone (α + β blocker)
- Block ↑ PVR (Vasodilator: Ca blocker, α blocker)
- Block RAAS system (Duretic, ACE inhibitor, ARB)
- Block Aldosterone system
Effects of Aging on HT
Systolic blood pressure:
- ↑ continuously
Diastolic blood pressure:
- ↑ then ↓
- ∵ ↑ then ↓ in arterial compliance (stiffness) —> ***compensating ↑ in SBP to maintain MAP
How to diagnose HT?
Optimal BP:
- <120/80
- Repeat BP every ***5 years
Normal BP:
- 120-129 / 80-84
- Repeat BP every ***3 years
Pre-HT / High-normal BP:
- 130-139 / 85-89
- Consider masked HT —> Out-of-office BP (**Ambulatory BPM / **Home BPM)
- Repeat ***annually
Hypertension:
- 140/90
- ***Reconfirm ↑ BP
—> Repeat visits for office BP measurement / Out-of-office BP (ABPM / HBPM)
***BP classification
Optimal: 120/80
Normal: 120-129 / 80-84
Pre-HT / High-normal (at-risk): **130-139 / **85-89
***記: 4,6,8 / 9,10,11
Grade 1 HT: 140-159 / 90-99
Grade 2 HT: 160-179 / 100-109
Grade 3 HT: >=180 / >=110
Isolated Systolic HT: >=140 / ***<90
Others:
- Office BP: >=140 / >=90
- ABPM:
—> 24-hour average: >=130 / >=80
—> day time average: >=135 / >=85
—> night time average: >=120 / >=70
- HBPM: >=135 / >=85
Home BP monitoring
Self-measurement of BP at home is of **clinical value + **demonstrated prognostic significance
- provide more info on BP lowering effect of treatment at **trough —> therapeutic coverage throughout dose-to-dose time interval
- **improve patients’ adherence to treatment
- doubts on technical reliability / environmental conditions of Ambulatory BP data
However discouraged when:
- causes **anxiety to patients
- induce **self-modification of treatment
Normal values are different for office and home BP (10 mmHg lower)
Good for:
- ***Pregnancy HT
Ambulatory BP monitoring
Indications:
- Considerable variability of office BP
- Marked discrepancy between office BP vs home BP
- Resistance HT
- ***Hypotensive episodes esp. in elderly and DM (i.e. Postural hypotension)
- Office BP elevated in pregnant women + pre-eclampsia suspected
Good for:
- White coat HT
- **Masked HT (much higher risk of CVS events than Uncontrolled HT)
- **Nocturnal HT
- Autonomic dysfunction
***HBPM vs ABPM
HBPM and ABPM more highly correlated with BP-related risk (LVH, Kidney damage)
- ***ABPM highest correlation
ABPM:
Advantages:
- White-coat, **Masked HT
- Stronger prognostic evidence
- **Night time readings
- Real-life setting
- **Additional prognostic BP phenotypes
- Abundant info from single measurement session including **short-term BP variability
Disadvantages:
- **Expensive
- Limited availability
- **Uncomfortable
HBPM:
Advantages:
- White-coat, **Masked HT
- **Cheap
- Widely available
- Measurement in home setting (more relaxed than office)
- **Patient engagement
- **Easily repeated, used over longer periods to assess ***day-to-day BP variability
Disadvantages:
- Only **static BP
- Potential for measurement error (∵ not calibrated)
- **No nocturnal readings
White coat HT
- Office BP persistently ↑
- Outside clinic BP normal (by ABPM / HBPM)
Prevalence:
- 15-30% of general population
- common in elderly / pregnant women
Risk:
- less than sustained HT
- slightly higher risk to normal people? Precursor to HT?
Implications:
- **No specific clinical characteristics
- Must be considered in people with newly diagnosed HT + before treatment, placed in context of overall risk profile
- Reassure patients, employers, insures that risk is low / absent
- **Close follow-up + monitor again
Evaluation of newly diagnosed HT
- Recent onset / exacerbation
- ***Secondary causes (Secondary HT)
- Family history
- Prior treatment for HT
- Past medical history
- Review of systems
- weight change
- anxiety disorders
- urinary tract obstruction
- ***sleep apnea
- sexual function - Personal history
- PE
- ***organ damage
- pre-existing risk factors
Aims:
- Confirm chronic elevation of BP + determine the level
- Uncovering correctable **secondary forms of HT
- Establishing pretreatment **baseline (RFT, Cardiac function)
- Assess factors influencing type of therapy / changed adversely by therapy
- Determine whether **target organ damage present
- Determine whether other risk factors for development of **atherosclerotic CVS diseases are present
S/S of HT
- None
- Elevated BP
- ***headache
- dizziness
- palpitations
- easy fatiguability
- impotence - Hypertensive vascular diseases
- **epistaxis
- haematuria
- blurring of vision
- episodes of weakness / dizziness
- **angina pectoris
- ***dyspnea - Underlying disease - ***Secondary HT
- Primary aldosteronism —> HypoK —> ADH resistance: polyuria, polydipsia, muscle weakness
***Investigations of Hypertension
- CVD risk factors
- HT
- smoking
- obesity (BMI >30)
- inactivity
- dyslipidaemia
- DM
- Microalbuminuria / eGFR <60
- age (male >55, female >65)
- family history
—> HT: Essential HT
—> **premature CVD (male <55, female <65)
—> **age onset: Secondary HT (35), delayed onset (>55)
- lifestyle
- duration + previous BP levels -
**Secondary causes
- **Renal
—> Parenchymal renal disease (e.g. glomerulonephritis, diabetic nephropathy, polycystic kidney)
—> Occlusive vascular disease (e.g. atherosclerotic obstruction of renal artery)
- **Adrenal (e.g. pheochromocytoma, primary hyperaldosteronism)
- **Neurogenic (e.g. brain tumour)
- Others (e.g. coarctation of aorta, pre-eclampsia, complete heart block, AR, PDA) - Target organ damage
Outcome:
- Assessment of Prognosis
Physical Examination of HT
- General appearance
- BP + Pulses
- in 2 upper extremities (arm + forearm)
- Supine + Standing - Height + Weight
- BMI
- Waist circumference - ***Fundi examination
- ***Peripheral arteries: Palpation + Auscultation
- CVS examination
Basic tests for initial evaluation
- Urine examination
- rule out renal diseases - ***Creatinine, Urea
- baseline kidney function
- rule out renal diseases - ***K, Ca
- hyperaldosteronism
- hyperparathyroidism - Glucose
- rule out DM - Total cholesterol, HDL, LDL, TG
- look for associated CVS risk factors - Serum uric acid
- baseline
- Gout - ***ECG
- LVH, MI, HF, Heart block - ***TSH
- rule out thyroid disorders - CXR
- Cardiomegaly, HF
Indications for looking for Secondary HT
- ***Younger patients (<40) with Grade 2 HT / onset of any grade of HT in childhood
- ***Acute worsening HT in patients with previously documented chronically stable normotension
- Resistant HT
- Severe (grade 3) HT / ***Hypertension emergency
- Presence of extensive ***HMOD (hypertension-mediated organ damage)
- Clinical / Biochemical features suggestive of **Endocrine causes of HT / **CKD
- Clinical features suggestive of ***OSAS
- Symptoms suggestive of ***Phaeochromocytoma / family history of Phaeochromocytoma
***Identifiable causes of HT
- A
- Accuracy of diagnosis
- Apnea: ***OSAS - B
- Bruit (**renal artery stenosis)
- Bad kidney (renal failure, **polycystic kidney) - C
- Catecholamine (**pheochromocytoma)
- **Cushing
- Coarctation of aorta - D
- Diet (salt, alcohol, obesity)
- ***Drugs (immunosuppressive agents, NSAID, estrogen, COC, weight-loss agents, stimulants, mineralocorticoids, anti-parkinsonian, MAOI, anabolic steroids, sympathomimetics, herbal) - E
- Erythropoietin
- ***Endocrine (primary / secondary hyperaldosteronism, hyper / hypothyroidism, parathyroid disease)
History taking for Secondary HT
- Polycystic kidney
- Family history of renal disease - Parenchymal renal disease
- renal disease, UTI, haematuria, analgesic abuse - Drug / substance intake
- OSAS
- snoring, daytime somnolence, obesity - Phaeochromocytoma
- sweating, headache, anxiety, palpitation - Aldosteronism
- ***muscle weakness (hypoK), tetany - Hyperparathyroidism
- hyperCa —> kidney stone, depression, lethargy, weakness - Hyperthyroidism
- heat intolerance, weight loss, tremor, palpitation - Hypothyroidism (hypercholesterolemia + ↑ PVR)
- fatigue, weight gain, hair loss, diastolic HT, weakness
Physical examination for Secondary HT
- Cushing
- Cushing features - Phaeochromocytoma
- skin stigmata of neurofibromatosis e.g. Cafe au lait spot - Polycystic kidney
- palpable enlarged kidney - Renovascular HT
- auscultation of abdominal murmurs - Aortic coarctation / Aortic disease
- auscultation of precordial / chest murmurs
- diminished + delayed femoral pulses, reduced femoral BP - Screening tests for Secondary HT (記)
- **Renal parenchymal disease
- **Primary aldosteronism
- **Renal artery stenosis
- **Pheochromocytoma
- **Cushing
- **Coarctation of aorta
- OSAS
- ***Thyroid disease
Renovascular HT
Cause:
- Renal artery stenosis
Medical history:
- DM
- Smoking
- Atherosclerotic disease
Investigations:
- **Duplex USG
- CT
- MRI
—> **Renal angiography
Findings:
- **Severe HT on ABPM
- **Reverse nocturnal dipping
- LVH, CAD
- Flash pulmonary edema
- **Impaired RFT
- **Secondary hyperaldosteronism
- Abdominal bruits
- Peripheral vascular disease
Treatment:
- ***Renal artery revascularisation (angioplasty)
Indications:
- Cardiac disturbance syndromes (flash pulmonary edema / ACS) with severe HT
- Resistant HT
- Ischaemic nephropathy with CKD
***ACE inhibitor may worsen kidney function in bilateral renal artery stenosis:
- ∵ ↓ efferent pressure —> cannot impedes blood out of glomerulus —> cannot maintain GFR —> renal failure
Mineralocorticoid HT
Cause:
- Hyperaldosteronism
Medical history:
- Fatigue
- Muscle weakness
- Polyuria
- Polydipsia
- Constipation
Investigations:
1. ↓ Renin, ↑ Aldosterone, ↑ ARR —> **Primary hyperaldosteronism
—> Confirmatory testing
—> Adrenal imaging (CT / MRI)
—> **Adrenal vein sampling (AVS)
—> ***Lateralisation
—> Yes: APA (Aldosterone-producing adenoma)
—> No: IHA (Idiopathic bilateral adrenal hyperplasia)
- ↑ Renin, ↑ Aldosterone, - Aldosterone-Renin ratio (ARR) —> Secondary hyperaldosteronism
- ↓ Renin, ↓ Aldosterone, - ARR —> Other disease
Findings:
- Severe HT
- ↓ Nocturnal dipping
- LVH, myocardial fibrosis
- **muscle weakness
- **Serum: ↑ Aldosterone, ↓ Renin, ↓ K, ↓ Mg, ↑ Na, Alkalosis (↓ H)
- Urine: ↑ Aldosterone, ↑ K, ↓ Na, ↓ pH (↑ H)
