Wednesday, 1 August 2012

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

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