Cardiology JC010: High Blood Pressure: Hypertension Flashcards

1
Q

Hypertension

A
  • 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

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2
Q

Burden of hypertension

A
  • 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
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3
Q

Consequences of HT

A
  1. ↑ Stroke risk
  2. ↑ Coronary artery disease risk (e.g. MI)

DBP: 90 (relative risk = 1, ∴ used as cutoff)

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4
Q

***Uncontrolled HT and Risk for CVS events

A

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

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5
Q

What cause “essential” HT?

A

Essential HT = Primary HT (vs Secondary HT)

No single risk factor for HT (for 90-95%)
1. Environmental
2. Genetic

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6
Q

Mechanisms of HT

A

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

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7
Q

Effects of Aging on HT

A

Systolic blood pressure:
- ↑ continuously

Diastolic blood pressure:
- ↑ then ↓
- ∵ ↑ then ↓ in arterial compliance (stiffness) —> ***compensating ↑ in SBP to maintain MAP

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8
Q

How to diagnose HT?

A

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)

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9
Q

***BP classification

A

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

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10
Q

Home BP monitoring

A

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

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11
Q

Ambulatory BP monitoring

A

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

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12
Q

***HBPM vs ABPM

A

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

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13
Q

White coat HT

A
  • 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

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14
Q

Evaluation of newly diagnosed HT

A
  1. Recent onset / exacerbation
  2. ***Secondary causes (Secondary HT)
  3. Family history
  4. Prior treatment for HT
  5. Past medical history
  6. Review of systems
    - weight change
    - anxiety disorders
    - urinary tract obstruction
    - ***sleep apnea
    - sexual function
  7. Personal history
  8. 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

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15
Q

S/S of HT

A
  1. None
  2. Elevated BP
    - ***headache
    - dizziness
    - palpitations
    - easy fatiguability
    - impotence
  3. Hypertensive vascular diseases
    - **epistaxis
    - haematuria
    - blurring of vision
    - episodes of weakness / dizziness
    - **
    angina pectoris
    - ***dyspnea
  4. Underlying disease - ***Secondary HT
    - Primary aldosteronism —> HypoK —> ADH resistance: polyuria, polydipsia, muscle weakness
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16
Q

***Investigations of Hypertension

A
  1. 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
  2. **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)
  3. Target organ damage

Outcome:
- Assessment of Prognosis

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17
Q

Physical Examination of HT

A
  1. General appearance
  2. BP + Pulses
    - in 2 upper extremities (arm + forearm)
    - Supine + Standing
  3. Height + Weight
    - BMI
    - Waist circumference
  4. ***Fundi examination
  5. ***Peripheral arteries: Palpation + Auscultation
  6. CVS examination
18
Q

Basic tests for initial evaluation

A
  1. Urine examination
    - rule out renal diseases
  2. ***Creatinine, Urea
    - baseline kidney function
    - rule out renal diseases
  3. ***K, Ca
    - hyperaldosteronism
    - hyperparathyroidism
  4. Glucose
    - rule out DM
  5. Total cholesterol, HDL, LDL, TG
    - look for associated CVS risk factors
  6. Serum uric acid
    - baseline
    - Gout
  7. ***ECG
    - LVH, MI, HF, Heart block
  8. ***TSH
    - rule out thyroid disorders
  9. CXR
    - Cardiomegaly, HF
19
Q

Indications for looking for Secondary HT

A
  1. ***Younger patients (<40) with Grade 2 HT / onset of any grade of HT in childhood
  2. ***Acute worsening HT in patients with previously documented chronically stable normotension
  3. Resistant HT
  4. Severe (grade 3) HT / ***Hypertension emergency
  5. Presence of extensive ***HMOD (hypertension-mediated organ damage)
  6. Clinical / Biochemical features suggestive of **Endocrine causes of HT / **CKD
  7. Clinical features suggestive of ***OSAS
  8. Symptoms suggestive of ***Phaeochromocytoma / family history of Phaeochromocytoma
20
Q

***Identifiable causes of HT

A
  1. A
    - Accuracy of diagnosis
    - Apnea: ***OSAS
  2. B
    - Bruit (**renal artery stenosis)
    - Bad kidney (renal failure, **
    polycystic kidney)
  3. C
    - Catecholamine (**pheochromocytoma)
    - **
    Cushing
    - Coarctation of aorta
  4. D
    - Diet (salt, alcohol, obesity)
    - ***Drugs (immunosuppressive agents, NSAID, estrogen, COC, weight-loss agents, stimulants, mineralocorticoids, anti-parkinsonian, MAOI, anabolic steroids, sympathomimetics, herbal)
  5. E
    - Erythropoietin
    - ***Endocrine (primary / secondary hyperaldosteronism, hyper / hypothyroidism, parathyroid disease)
21
Q

History taking for Secondary HT

A
  1. Polycystic kidney
    - Family history of renal disease
  2. Parenchymal renal disease
    - renal disease, UTI, haematuria, analgesic abuse
  3. Drug / substance intake
  4. OSAS
    - snoring, daytime somnolence, obesity
  5. Phaeochromocytoma
    - sweating, headache, anxiety, palpitation
  6. Aldosteronism
    - ***muscle weakness (hypoK), tetany
  7. Hyperparathyroidism
    - hyperCa —> kidney stone, depression, lethargy, weakness
  8. Hyperthyroidism
    - heat intolerance, weight loss, tremor, palpitation
  9. Hypothyroidism (hypercholesterolemia + ↑ PVR)
    - fatigue, weight gain, hair loss, diastolic HT, weakness
22
Q

Physical examination for Secondary HT

A
  1. Cushing
    - Cushing features
  2. Phaeochromocytoma
    - skin stigmata of neurofibromatosis e.g. Cafe au lait spot
  3. Polycystic kidney
    - palpable enlarged kidney
  4. Renovascular HT
    - auscultation of abdominal murmurs
  5. Aortic coarctation / Aortic disease
    - auscultation of precordial / chest murmurs
    - diminished + delayed femoral pulses, reduced femoral BP
  6. Screening tests for Secondary HT (記)
    - **Renal parenchymal disease
    - **
    Primary aldosteronism
    - **Renal artery stenosis
    - **
    Pheochromocytoma
    - **Cushing
    - **
    Coarctation of aorta
    - OSAS
    - ***Thyroid disease
23
Q

Renovascular HT

A

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

24
Q

Mineralocorticoid HT

A

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)

  1. ↑ Renin, ↑ Aldosterone, - Aldosterone-Renin ratio (ARR) —> Secondary hyperaldosteronism
  2. ↓ 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)

25
Q

OSAS

A

Medical history:
- snoring
- exaggerated daytime sleepiness
- morning headache
- lack of concentration
- irritability
- ↑ frequency of motor vehicle accidents

Investigations:
- **Epworth sleepiness scale
- **
Polysomnography (AHI)

Findings:
- narrow upper airway
- **non-dipper in nocturnal BP
- **
LVH, Cor pulmonale
- ***Pulmonary hypertension
- obesity
- peripheral edema

Treatment:
- weight reduction
- ***CPAP
- mandibular advancement splints

26
Q

Target organ damage

A

記5樣: 腦, 眼, 心, 腎, 血管

  1. Brain
    - headache, vertigo, impaired vision, ***TIA, sensory / motor deficits
    —> Murmurs over neck arteries, sensory / motor deficits
  2. Eyes
    - narrowing of retinal artery
    —> ***Fundoscopic abnormalities (Retinal exudates, haemorrhages, papilloedema)
  3. Heart
    - palpitation, chest pain, SOB, swollen ankles
    —> Location + characteristics of ***apical impulse
    —> Abnormal cardiac rhythms
    —> Ventricular gallop
    —> Pulmonary rales
    —> Peripheral edema
  • **LVH, **Diastolic dysfunction
    —> ECG, ***Echo, CXR
  1. Kidney
    - thirst, polyuria, nocturia, haematuria, proteinuria
    —> **Serum creatinine level, **Dipstix
  2. ***Peripheral arteries
    - cold extremities
    - intermittent claudication
    —> Absence, reduction, asymmetry of pulses
    —> Cold extremities
    —> Ischaemic skin lesions
  3. Large arteries
    - Carotid, Aorta, Iliac, Femoral atherosclerotic plaques
    —> **Systolic murmurs
    —> **
    USG
27
Q

Risk factors for ***Poor prognosis in HT

A

Concomitant CVS risk factors:
1. **Black
2. **
Youth
3. ***Male
4. Persistent DBP >115
5. Smoking
6. DM
7. Hypercholesterolaemia
8. Obesity
9. Excess alcohol

Target organ damage:
10. ***Evidence of end organ damage
- Heart: Cardiac enlargement, Ischaemia / LV strain, MI, CHF
- Eyes: Retinal exudates, haemorrhages, papilloedema
- Renal: Impaired RFT
- Brain: Cerebrovascular accident

28
Q

DM and HT

A

Risks:
Kidney: ↑ CKD
Heart: ↑ CHD, LVH, CHF
Brain: ↑ stroke

29
Q

Goal of Therapy

A
  1. Achieve max reduction in total risk of CVD
    - need for treatment of other risk factors + BP control
  2. Achieve optimal / normal BP
    - young, middle aged, DM patients: <= 140 / 80-85
    - high-normal BP in elderly: <= 140-150 / 90
  3. Successful management = Good communication + relationship
    - ∵ hypertensive treatment is for life
30
Q

***Treatment of HT

A
  1. BP above goal?
    - No: Lifestyle modification
    - Yes: Initial drug treatment + Treat other CVS risk factors
  2. Drug treatment
    - Choose based on **Compelling indication / **CI
    —> if BP not at / below goal
    —> Add other agent

No Compelling indication —> ***ABCD
- ACEI / ARB
- β-blocker
- CCB
- Diuretic
—> Single agent / Fixed dose combination (esp. for stage 2 HT)

  1. No improvement
    —> ***Maximise first medication, Add 2nd medication before max dose, Start with 2 classes separately / fixed-dose combination
  2. Still no improvement
    - Treatment resistance
    —> exclude Pseudoresistance (AT-GOALs) (using HBPM / ABPM)
    —> Adherence
    —> Timing of drug
    —> Greater dose of medication
    —> Other class: Diuretic, add **Aldosterone antagonist (Spironolactone)
    —> Alternative Rx: use combination with different action, **
    Loop diuretic in patients with renal disease +/- potent Vasodilator
    —> Look for contributing factors (high salt diet, obesity, reduce interfering agents e.g. NSAID, OC pill etc.)
    —> Look for Secondary HT
    —> Referral
31
Q

Lifestyle modifications

A

Normotensive individuals
- Prevent onset of HT
- ↓ BP —> ↓ CVS risk

Hypertensive patients:
- Serve as initial therapy before medication
- Adjunct to medication
- Facilitate medication step-down / withdrawal in certain individuals
- ↓ CVS risk

  1. Diet control (***Low Na, Low calorie)
  2. Low fat diet, rich in fruit, vegetable (***DASH diet)
  3. Weight loss
  4. Regular exercise
  5. Moderation of alcohol consumption <2 drinks / day
  6. Reduce consumption of coffee, green, black tea
  7. Smoking cessation
  8. Reduce stress
  9. Reduce exposure to air pollution / cold temperature
  10. Complementary, alternative, tradition medicines
32
Q

Indications and Goals of Pharmacological therapy

A

Indications:
- Resistant HT despite lifestyle modification
- High CVD risk factors
—> Stage 2 (asymptomatic + HMOD, CKD grade 3, DM without organ damage)
—> Stage 3 (symptomatic + symptomatic CVD, CKD >=4, DM with organ damage)

**Treatment goal:
- 18-65: <130 (CKD <140)
- <80 yo: <140/90 (H/ABPM: <135/85)
- >80 yo: <150/90 (H/ABPM: <145/85)
- **
High risk: <120
- ***DM: <130/80
- All other: <140/90
- Optimal range: 120-140 / 70-80

Interventions to improve compliance:
- record medicine taking
- encourage people to monitor their condition
- simplify regimen
- alternative packaging
- multi-compartment medicines system

Too aggressive BP lowering (<120 / 70) (J-curve):
- ↓ Organ perfusion

33
Q

***Pharmacological therapy

A

記: ACD —> B (add when indicated) —> Spironolactone, α blocker, Vasodilator

No Compelling indication (***ACD):
1. Single drug
- ACEI / ARB
- CCB
- Thiazide

  1. Two drugs
    - ACEI / ARB + CCB
    - ACEI / ARB + Thiazide
    - CCB + Thiazide

With Compelling indication:
1. DM
- ACEI / ARB
—> Add-on: Thiazide —> β-blocker / CCB

  1. CKD
    - ACEI / ARB
  2. CAD
    - ACEI / ARB + ***β-blocker
    —> Add-on: Aldosterone antagonist, CCB, Thiazide
  3. LV dysfunction
    - ACEI / ARB + β-blocker + ***Diuretic
    —> Add-on: Aldosterone antagonist / Hydralazine + Isosorbide dinitrate
  4. Previous ischaemic stroke
    - ACEI +/- Thiazide

Regimen:
1. Initial therapy
- Dual combination: ACEI / ARB + CCB / Diuretic
- Monotherapy (low-risk grade 1 HT / very old patients)

  1. Step 2 (Triple combination):
    - ACEI / ARB + CCB + Diuretic
  2. Step 3 (Triple combination + Spironolactone / other drugs):
    - add **Spironolactone / other Diuretic, **α / β-blocker
    - consider referral to specialist for further investigation

**β-blocker: consider at any stage if have specific indication e.g. **HF, **angina, post-MI, **AF, younger women / planning pregnancy

Combination therapy:
- synergistic effect
- act on different mechanisms
- counteract adverse effects
—> CCB: tachycardia + β-blocker: bradycardia
—> CCB: ankle edema + Thiazide: remove water
—> ACEI: hypoNa + Thiazide: add Na

2nd line agents:
1. α-blocker
2. Aldosterone antagonist (Spironolactone, Eplerenone)
3. Vasodilator

34
Q

CI to specific drugs

A

Diuretics (Thiazides):
- ***Gout
- HypoK
- HyperCa

β-blockers:
- **Asthma
- **
High-grade SA / AV block
- ***Bradycardia (HR <60)

CCB (Dihydropyridines):
- Tachyarrhythmia

CCB (Verapamil, Diltiazem):
- **High-grade SA / AV block
- **
Severe LV dysfunction (LV ejection fraction <40%)
- Bradycardia (HR <60)

ACEI:
- **Pregnancy (fetal hypotension, renal failure, oligohydramnios, malformation, death)
- Previous angioneurotic edema
- **
HyperK (>5.5)
- ***Bilateral renal artery stenosis

ARB
- Pregnancy
- HyperK (>5.5)
- Bilateral renal artery stenosis

35
Q

SE of drugs

A
  1. Diuretic
    - Hypo/HyperK
    - HypoNa
    - HypoMg
    - dehydration / **postural hypotension
    - **
    gout exacerbation (hyperuricaemia) (esp. Thiazide)
  2. Aldosterone antagonist
    - **HyperK
    - HypoNa
    - dehydration / postural hypotension
    - **
    Gynaecomastia (Spironolactone)
  3. ACEI
    - **dry cough
    - **
    HyperK
    - **renal failure in bilateral renal artery stenosis
    - **
    angioedema (∵ bradykinin)
  4. ARB
    - HyperK
    - renal failure in bilateral renal artery stenosis
  5. CCB Dihydropyridine
    - **tachycardia
    - **
    peripheral edema
    - ***flushing (vasodilation)
    - worsening GERD
  6. CCB Non-dihydropyridine
    - ***heart block
    - peripheral edema
    - constipation
    - worsening GERD
  7. β-blocker
    - exercise intolerance
    - fatigue
    - **heart block
    - **
    exacerbation of peripheral arterial disease
    - erectile dysfunction
    - ***masking S/S of hypoglycaemia (hypoglycaemia-induced tachycardia)
36
Q

Monitoring to drugs

A
  1. Diuretic
    - BP
    - BUN / creatinine
    - **electrolyte
    - **
    uric acid (esp. Thiazide)
  2. Aldosterone antagonist
    - BP
    - BUN / creatinine
    - ***K
  3. ACEI / ARB
    - BP
    - BUN / creatinine
    - ***K
  4. CCB Dihydropyridine / Non-dihydropyridine
    - BP
    - ***HR
  5. β-blocker
    - BP
    - ***HR
37
Q

Malignant HT

A

Marked BP ↑ (***DBP > 140) with encephalopathy / nephropathy / papilloedema +/- microangiopathic haemolytic anaemia

  • <1% of HT population
  • 25-50% 5-year mortality

S/S (End-organ damage):
1. **Eyes: Papilloedema, Retinal haemorrhage, exudates
2. Brain: **
HT encephalopathy: severe headache, vomiting, visual disturbance (transient blindness), transient paralysis, convulsions, stupor, coma
3. Heart: Cardiac **decompensation
4. Kidney: **
Acute renal failure with oliguria

(MAHA in Malignant hypertension: (Web)
- disruption of vascular endothelium, causing fibrinoid materials to enter the vascular wall and obliterate the vascular lumen)

38
Q

Indications for immediate / early treatment for hypertension

A

Hypertensive emergency (immediate Rx within **1 hour)
- Malignant HT
- **
HT encephalopathy
- **Acute HF
- Unstable angina / MI
- **
Dissecting aortic aneurysm
- **Cerebral haemorrhage
- **
Renal failure
- Severe pre-eclampsia
- Adrenergic crisis
—> ***IV drugs

Hypertensive urgency (early Rx within ***24 hours)
- HT with grade 3 / 4 retinal changes
- Severe pre-op / peri-op HT

39
Q

Indications for Emergency reduction of BP with IV treatment

A
  1. Hypertensive encephalopathy
    - Malignant HT
    - Eclampsia
  2. Acute LVF due to HT
  3. ***Dissecting aneurysm

Emergency reduction of BP in some conditions e.g. Accelerated BP associated with acute stroke is contraindicated
- loss of cerebral **autoregulation —> consequent risk of cerebral **infarctions

40
Q

Treatment of Hypertensive emergency

A

Acute aortic dissection:
- Nitroprusside (NO: vasodilation) + **Metoprolol (β1-blocker)
- **
Labetalol (β-blocker + α1-blocker (vasodilation effect): α+β blockade)

Pheochromocytoma crisis:
- Phentolamine (α-blocker) / Urapidil (α-blocker)
- Nitroprusside (NO: vasodilation)

41
Q

Case 1:
- 57 yo female
- ↑ BP (155/95)
- no Hx of CVS disease
- Hx of gout not on regular Rx
- gained 15lb in last 5 years
- 86kg, 165 cm (BMI: 31)
- waist circumference 95cm

A

P/E:
- Fundoscopy: NAD
- CVS, Abdominal exam: normal
- Urine: NAD

Investigations:
- RFT: normal
- FBS: 6.2 mmol / L (↑)
- Lipid: TG 2, HDL 1, LDL 2.6, Urate 600 (↑)
- ECG: NAD

Diagnosis:
- Essential HT + Metabolic syndrome

Treatment:
- Diet control + Lifestyle modification —> No change in body weight —> 150/94, HR 60bpm
—> Pharmacological treatment (also emphasis on diet / weight control)

Start on ACEI
- avoid β-blocker (∵ HR 60, bradycardia)
- avoid Diuretic (∵ gout)
- advice further diet control + lifestyle modification
—> weight loss 2kg but BP still high 145/90
—> Add CCB / ↑ ACEI
—> still no improvement after 4 weeks
—> Treatment failure? Non-compliance?
—> Include Thiazide unless CI + Add 2nd line agents (α-blocker, Aldosterone blocker, Vasodilator)

Defaulted follow up with poor compliance to medications due to cough after ACEI
- 18 months with SOB
- BP 220/130, ankle edema, bilateral crepitation
—> Malignant HT

42
Q

Additional notes

A

Celecoxib:
- Antagonise RAAS inhibitors / Beta-blockers
—> Worsen BP control

Non-selective COX / COX-2 inhibitor:
- ↓ Prostanoid formation
—> ***Vasoconstriction (cause Renal insufficiency —> Renal impairment)