Hypertension Part 3: When to intervene

High Blood pressure is a major risk factor for cardiovascular disease. None the less it is important to consider any individual risk factor in the context of overall cardiovascular risk.
treatment is influenced by

• pre-existing vascular disease
• other risk factors
• associated conditions (diabetes and renal disease) & target organ damage

Treatment Goals

• improve long term survival and quality of life
• reduce blood pressure
• reduce overall cardiovascular risk
• minimise end-organ damage

"Remember to remove, revise, or substitude drugs which may be causing hypertension (eg NSAIDs, corticosteroids, oral contraceptives)" Murtagh's General Practice 5th edition.


Individual and population interventions to reduce blood pressure, stroke and vascular disease (From Medicine Today sept 2009 vol 10 number 9 p 62; and Guidelines for the management of absolute cardiovascular disease risk p 39)

• decrease weight (ideal weight is BMI <25 and waist circ < 94 cm in men (<90 Asian men) and < 80cm in women (including Asian women).
• physical exercise (minimum 30 mins 5 to 7 times a week)
• reduce salt < 6 grams a day (= 2300 mg sodium)
• reduce alcohol (<2 drinks a day and 2 alcohol free days)
• increase unsaturated fat intake
• increase fresh fruit and vegetable intake
• use drug therapy in high risk individuals
• no smoking 

Immediate treatment to lower blood pressure is recommended in the following situations:

• Systolic blood pressure 180 mmHg or greater (grade 3 hypertension) and or
• Diastolic blood pressure 110 mmHg or greater
• Systolic blood pressure 160 mmHg or greater and diastolic blood pressure 70 mmHg or less (isolated systolic hypertension with widened pulse pressure)
• Patients with associated conditions (for example, stroke or myocardial infarction) or evidence of end-organ damage (for example, microalbuminuria, left ventricular hypertrophy) also need urgent treatment (see the tables below)
• Patients assessed as being at "high risk" following 5 year absolute risk assessment

Any pharmacotherapy should always be used in conjunction with lifestyle modification, and management of associated conditions.

 

 

Associated clinical conditions
Diabetes	Ø  > age 60 Ø  With urine ACR >2.5 male or > 3.5 female
Cerebrovascular disease	Ø  Ischaemic or haemorrhagic stroke Ø  TIA
Coronary heart disease	Ø  MI Ø  Angina Ø  Stent/ angioplasty
Chronic heart failure
Chronic kidney disease	Ø  Diabetic nephropathy Ø  GN Ø  Hypertensive kidney disease
Aortic disease	Aneurism (dissecting or fusiform)
Peripheral Arterial Disease	Clinically or ABI < 0.9
Hypercholesterolaemia	>7.5 total
Family history of:	Premature cardiovascular disease
Previous diagnosis of:	Familial hypercholesterolaemia

End Organ Disease
LVH	Diagnosed on ECG or echo (see previous blog)
Microalbuminuria
Chronic kidney disease	Presence of either Ø  Proteinuria Ø  eGFR < 60
Vascular disease	Ø  Atherosclerosis evident on ultrasound or radiology Ø  Hypertensive retinopathy grade II or higher

From Heart Foundation Guide to Management 2010 guide

The most up to date guidelines on blood pressure that I can find are the "National Vascular Disease Prevention Alliance Guidelines for the management of absolute cardiovascular disease risk". 2012.

In contrast to the 2008 (updated 2010) guidelines from the Heart Foundation "Guide to the Management of Hypertension", the former, more recent guidelines, recommend immediately treating anyone who is over age 45, at low or moderate risk (based on the Australian cardiovascular risk charts) with blood pressure ≥ 160/100.

Treatment should begin with any of the following

• ACEi or ARB
• CCB (dihydropyridine)
• Low dose thiazide or thiazide like diuretic (in patients > age 65)*

* Note that thiazide diuretics have been associated with increased risk of new onset diabetes therefore use cautiously in patients with "pre-diabetes" or metabolic syndrome. The Heart foundation recommends reserving these agents as first-line for older patients in whom the benefits of managing isolated systolic hypertension and preventing stroke are likely to outweigh the risk of diabetes onset.

Always begin with the LOWEST recommended dose (e.g. ACEi or ARB).

If target not reached after 6 week trial

suggest ACEi (or ARB) + CCB (dihydropyridine)

If target not reached at 3 months

suggest ACEi (or ARB) + CCB + Thiazide

ACEi/ ARB are recommended in a number of settings for cardiac and renal benefit, they must be used cautiously/ avoided in patients with renal artery stenosis.

Beta Blockers are recommended post MI and in the setting of angina. Exercise caution in patients with depression, uncontrolled heart failure, bradycardia/ AV block and asthma/ COPD.

Combinations to avoid:

X ACEi (or ARB) + potassium sparing diuretic (spironolactone, amiloride)

= hyperkalaemia

X Beta blocker + verapamil 

= heart block

X ACEi + ARB

= hypotension and lack of efficacy

Common Adverse Effects

 ACEi (and ? ARB) can cause cough
CCBs may cause constipation (especially verapamil), flushing, headache and oedema
Thiazide diuretics can cause gout
Beta blockers can cause depression, lethargy, erectile dysfunction

If blood pressure is not responding to medication, reassess for;

• non adherence
• undiagnosed secondary cause
• hypertensive effects of other drugs
• treatment resistance due to sleep apnoea
• hidden use of alcohol or recreational drugs
• unrecognised high salt intake
• white coat hypertension
• technical factors affecting measurement
• volume overload in CCF

Which of the following  combinations would you avoid?

• Lisinopril 20mg daily and Olmesartan 30mg once daily
• Eplerenone 50mg and Captopril 25mg
• Atenolol 50mg daily and Verapamil CR 240mg once daily
• Carvedilol 50mg and Amlodipine 10mg in a patient with CHD

Following blogs will cover management of hypertension in particular situations such as pregnancy, diabetes, stroke etc





Blood Pressure Part 2

Case Study

 

Mr Lim is a 55 year old, newly retired English professor. He has recently moved to the area with his wife, May-Ling. His wife was recently diagnosed with hypertension and had been attending a local nurse-run clinic to have her blood pressure monitored. The nurse checked Mr Lim's blood pressure last month, and told him it was high. Since that time they bought a blood pressure monitor and have been checking it every day at home, having been shown how to do so by the nurse. The readings are between 139/ 90 to 152/100.

 

How would you assess him, and what are you looking for?

 

In all patients with confirmed hypertension, assessment includes:

• Careful history
• Physical examination
• Initial investigations
• Further investigations as required

Assessment is aimed at

1. identifying all risk factors
2. detecting end organ damage
3. detecting related or co-morbid clinical conditions
4. identifying causes of secondary hypertension

To help you recall the above remember SCoRE

Secondary hypertension

Co-morbid conditions
Risk factors
End organ damage

 

Two important causes of secondary hypertension are sleep apnoea (enquire about snoring especially in an overweight patient) and phaeochromocytoma (headache, sweating, palpitations). 

 

Medications can increase BP also. Some common ones in general practice include monoamine oxidase inhibitors (moclobemide), prednisolone, clozapine, NSAIDs, oral contraceptives and (the nasty) sibutramine. Complementary meds to watch for include ginger, ginseng, caffeine, melatonin and St John's wart.

 

When asking about important co-morbid conditions, remember ABDCEFG

Apnoea (sleep apnoea), Asthma, diaBetes, COPD, Dyslipidaemia, Erectile dysFunction, Gout

 

And don't forget the all important modifyable risk factors SNAP BBL

 

Smoking, Nutrition (salt, saturated fat), Alcohol (and other drugs such as amphetamines, cocaine), Physical Activity (and obesity), Blood pressure, BMI (and waist circ) and lipids (if not already covered).

 

When asking about past history (ie assessment of end organ damage), remember "brain, heart, kidneys, peripheries". And think about the typical "vasculopath". You need to enquire about past history or current symptoms of:

• cerebrovascular disease
• ischaemic heart disease
• heart failure
• peripheral arterial disease
• chronic kidney disease

You might ask...
" Have you ever had a blood clot in your brain, or a stroke? Have you ever had a heart attack or chest pain? Have you ever woken up gasping for breath or do you need to sleep sitting up? Have had trouble with your kidneys or noticed you wee a lot at night or your urine has gone a dark colour? Have you ever had problems with blood flow to your legs, leg ulcers, or cramps in your legs when you exercise?"

 

Remember that leg cramps, muscle weakness or cardiac arrhythmias may also be an important indicator of hypokalaemia. If this is the case look for U waves on the ECG.

 

 

Here is a picture* to help you remember...

 

 

 

 

(*The reference for the original picture is Clinically Oriented Anatomy 6th ed by Moore, Dally & Agur)

 

 

To complete your evaluation of a patient with hypertension, include family history (BP, diabetes etc) and psycho-social health.

 

 

List 7 errors GP's commonly make when taking a patient's blood pressure

1. cuff placed over clothing
2. incorrect cuff size
3. arm elevated above the heart
4. failure to check that both arms give a similar reading at the first visit
5. patient talking during the measurement
6. rounding off the reading by more than 2mm Hg
7. deflating the cuff to quickly

(I never used to pay much attention to these factors until I discovered that the recordings I was getting for my patients were about 10 - 20 points different from mercury devices used at a local clinic. After much investigating, I discovered that the level of the arm, whether a patient talks etc all make a notable difference!)

 

 

Mr Lim's wife wants to know why it matters if blood pressure is high. "He doesn't feel any different to normal so what's the problem?" she asks.

 

Higher levels of blood pressure are strongly associated with increasing rates of cardiovascular disease, cardiovascular events, and death. Studies have shown that the lower the BP, the lower the risk of stroke, heart disease, kidney disease, heart failure and death.

 

 

After your thorough explanation they both ask what the difference is between the "top number and the bottom number" and which is more important.

 

Systolic blood pressure is a stronger and more consistent predictor or cardiovascular events such as stroke than diastolic BP.

 

 

Mr Lim is anxious now that you have conscientiously advised him that higher levels of blood pressure are associated with increased rates of cardiovascular events and death. He wonders whether he needs to come back to see you tomorrow for another assessment. How do you determine when to review?

Reassess BP regularly, at intervals determined by both the BP category (see the previous blog) and the patient's absolute cardiovascular risk (determined by the Framingham calculation).

 

 

When would lower than usual blood pressure targets be recommended?

Lower targets and initiation of antihypertensive therapy is recommended for all patients with blood pressure sensitive conditions (e.g. stroke, diabetes and CKD) even if BP is within the "normal range".

 

 

Treatment Target Summary

 

From table 6. Heart Foundation Guide to Management of Hypertension 2008. Updated 2010

 

 

 

 

NB there is a difference in the recommendations between those of the Australian Heart Foundation who suggest a patient with CKD should aim for BP <130/80 and Kidney Health Australia who suggest in "CKD management 2nd edition 2012) that targets for patients with CKD should be <140/90 unless diabetes or albuminuria are present in which case the goal is <130/80.

True or false? Treatment should be based on the BP readings you record in your clinic since ambulatory recordings at the patients home are subject to error.

 

 

see the bottom of the blog for the answer...

 

 

Mr Lim wants to know what has caused his hypertension. He is concerned that there may be an underlying medical condition and that treating his blood pressure might just "cover up" a more important problem. "How do I know there's not something else the matter with my body. What if my body's trying to tell me something's wrong?" He asks. 

 

You won't be able to answer if you don't understand the definition and classification of hypertension. A thorough assessment also requires a good working knowledge of the causes of secondary hypertension.

 

Hypertension is either essential  (95% of cases) or secondary. Essential hypertension is the presence of sustained hypertension in the absence of underlying, potentially correctable kidney, adrenal, or other other factors.

 

 

Causes of secondary hypertension include:

• Kidney (most common culprit)
• Glomerulonephritis
• reflux nephropathy (often associated w pyelonephritis)
• renal artery stenosis (artherosclerosis/ fibromuscular dysplasia)
• diabetes
• Endocrine
• Primary aldosteronism ("Conn's")
• Cushing's Syndrome (truncal obesity & pigmented striae)
• Phaeochromocytoma (sweaty, pale, palpitating)
• Oral Contraceptives
• Coarctation of the aorta (delayed femoral pulses)
• Immune disorders (eg PAN)
• Drugs
• Pregnancy

 

The patient with newly diagnosed hypertension needs a thorough physical examination with a cardiovascular focus. This does not mean a quick listen to the heart and blood pressure. See Talley and O'Connor 's Clinical Examination 6th edition as a guide.

 

Here is an example proforma:

 

 

 

 

The mnemonic ABCDE can be used to help determine secondary causes in the patient with elevated blood pressure:

 

Apnoea: Obstructive sleep apnoea is an independent risk factor for hypertension
Aldosteronism: Primary hyperaldosteronism is defined as overproduction of aldosterone. Too much salt and water is retained, leading to suppression of renin. (NB high renin is found in secondary hyperaldosteronism.) Potassium secretion is increased, so the patient has

↑ Na, ↑ serum and urine aldosterone, ↓K, ↓ plasma renin

Catecholamines
Coarctation
Cushing's
Diet (salt etc)
Drugs (NSAIDs, oestrogen etc)
Endocrine disorders
(Reproduced from AAFP http://www.aafp.org/afp/2003/0101/p67.html)

 

Clinical Features Suggesting Secondary Hypertension (From John Murtagh's General Practice 4th ed)

Clinical features	Likely source
Abdominal Bruit	Renal artery stenosis
Bilateral renal masses +/- haematuria	GN
Hx of claudication & delayed femoral pulse	Polycystic kidney disease
Progressive nocturia, weakness	Coarctation of the aorta
Paroxysmal hypertension with headache, pallor, sweating	phaeochromocytoma

Routine investigations

• Dipstick testing of urine for blood and protein
• Urinary albumin creatinine ratio.

Proteinuria: small amounts of protein are normally excreted in the urine (about 80mg/ day) and comprise filtered plasma proteins (albumin and low molecular weight immunoglobulin) and secreted tubular proteins. There are no official Australian standards for proteinuria and the cut-off for abnormal varies between 150-300 mg/day, depending on the laboratory.

Albuminuria: The normal mean value for urine albumin excretion is 10 mg/day but is increased by many physiological variables including exercise, fever, upright posture and

pregnancy. Microalbuminuria is defined as a range from 30-300 mg/day. Macroalbuminuria is defined as above 300 mg/day. (see www.cari.org.au)

Because protein excretion varies throughout the day, the normal ratio varies throughout the day. The ratio in a first morning specimen correlates most closely with overnight protein excretion rate, whereas the ratio in mid-morning specimens correlates most closely with 24-hour protein excretion rate. Creatinine excretion is  normally higher in men than women; therefore, the cut-off values for abnormalities in urine albumin-to-creatinine ratio are lower for men than women.

 

 

 

 Routine Investigations continued

• serology for fasting cholesterol, fasting glucose, UEC (urea, electrolytes, creatinine and eGFR), FBC (full blood count), uric acid, urea, liver function tests.
• ECG to look for LVH, IHD, conduction abnormalities.

What ECG finding is associated with increased cardiovascular risk?

"The presence of LV strain pattern (ST depression and T-wave inversion) is associated with increased cardiovascular risk in patients with hypertension"  (Heart Foundation Guide to the Management of Hypertension 2008.)
NB T wave inversion in V1 to V3 is normal.

A 70-year-old man with longstanding hypertension

Note the axis deviated to the left (don't be confused by the ventricular premature beats)
Note the S in V1 and the R in V6 (Left ventricular hypertrophy)
Note the widespread ST depression and T wave inversion

for a great summary of ECG axis and other things see http://lifeinthefastlane.com/ecg-library/basics/left-axis-deviation/

 

Further Investigations

• Echocardiogram if you are concerned about LVH (LVH is a marker of end organ damages and requires close follow up)
• Ankle-Brachial Index for any one at risk of PVD (e.g. smokers, diabetes, vascular bruits, older age). A score of < 0.9 is diagnostic. There is an MBS item number for performing an ABI.
• Carotid doppler if TIA suspected or if carotid bruits
• Plasma aldosterone/ renin ratio. Primary aldosteronism occurs in 5% to 10% of patients with hypertension and is not excluded by a normal serum potassium. Consider testing in all patients with treatment resistant hypertension +/- low serum potassium.
• Consider 24 hour urinary catecholamine, metanephrine adn normetanephrine in patients with symptoms of episodic catecholamine excess or episodic hypertension.
• Consider a renal artery ultrasound or renal CT angiogram in young females with hypertension, in patients with a renal bruit, or those who may have arthersclerotic renal artery disease. (Fibromuscular dysplasia is a significant cause of renal artery stenosis and hypertension in young females).

 

 

 

True or false? Treatment should be based on the BP readings you record in your clinic since ambulatory recordings at the patients home are subject to error.

 

 

False. "treatment decisions should be based on ambulatory BP, because end organ disease and cardiovascular event rates correlate more closely with ambulatory BP than with clinic readings. Also, night time (asleep) BP recordings may be a stronger predictor of cardiovascular events than day time (awake) BP. See page 6 of the "Heart Foundation Guide to Management of Hypertension 2008".

 

 

When to intervene in patients with confirmed hypertension will be covered in coming blogs.
Most of the details from today's blog have come from:

• "Heart Foundation Guide to Management of Hypertension 2008" Updated 2010
• "CKD Management in General practice 2012" 
• "John Murtagh's General Practice" 4th edition by John Murtagh